Antimicrobial resistance (AMR) has become a pressing need to address in the major global public health challenges, posing a serious threat to human health. Pseudomonas aeruginosa (PA) is one of the most concerning Gram-negative pathogens and is typically treated with broad-spectrum antibiotics. PA exhibits resistance to multiple antibiotics, multifactorial virulence, and dynamic hyperadaptation, which results in a particularly formidable challenge in eliminating PA from patients. The problem of drug resistance is becoming increasingly serious, and the development of new antibiotics is extremely lagging behind, resulting in no drug with a new structure and mechanism being approved for the treatment of infections caused by drug-resistant Gram-negative bacteria over the past half-century. Consequently, the development of new antibiotics is of utmost urgency and importance. Marine natural products (MNPs) have become an important source for developing new antibiotics due to their unique properties. So far, 44 potential molecules with significant anti-PA activity have been isolated from marine organisms, of which 19 have been reported as quorum-sensing system inhibitors (QSIs) with potential for further development. In this review, we provide a comprehensive summary of the current status of drug resistance, pathogenic mechanisms, and resistance mechanisms associated with PA infections. We also highlight the challenges and opportunities presented by MNPs in the development of anti-PA drugs, and offer recommendations to accelerate the antibiotic development process, thereby providing valuable insights for the study and exploitation of novel antibiotics.

Antibiotic use is known to contribute to the development of osteoporosis, although the exact mechanisms remain poorly understood. Metronidazole (MET), a commonly prescribed antibiotic for treating anaerobic infections, has been linked to alterations in the gut microbiota (GM), which in turn are associated with various adverse side effects in the host. Recent studies have shown that the GM plays a key role in regulating bone homeostasis, though the underlying mechanisms remain under investigation. In this study, we demonstrate for the first time that MET promotes inflammatory osteoporosis through gut dysbiosis, with Klebsiella variicola (K. variicola) identified as a major pathogen influencing bone metabolism. The pro-inflammatory extracellular vesicles (EVs) secreted by K. variicola induce enhanced inflammatory responses and osteoclastic differentiation in both bone macrophages and bone tissue. Notably, the use of antibiotics that target K. variicola effectively mitigates MET-induced bone loss in vivo. This study expands our understanding of the mechanisms underlying antibiotic-induced bone loss and underscores the significant role of the pathogenic bacterium K. variicola in the development of osteoporosis, providing new avenues for future research on the microbiota-gut-bone axis in bone-related diseases.

Historically, the management of acute uncomplicated diverticulitis was centered on antibiotics. However, modern theories regarding the pathogenesis of diverticulitis have challenged the notion that antibiotics are necessary in all cases. Despite major reform in many societal guidelines, the adoption of non-antibiotic therapy for uncomplicated diverticulitis has been limited, especially in North America. The purpose of this SAGES White Paper was to review the available evidence on antibiotic omission in uncomplicated diverticulitis and to explore methods of safe implementation.

A task force within the SAGES Colorectal Surgery Committee was formed to work on this White Paper. The committee and its leadership approved an outline that would focus on the following topics: (1) Defining the problem with unnecessary antibiotic exposure; (2) Evaluating the evidence on antibiotic omission in uncomplicated diverticulitis; (3) Identifying the appropriate patient for antibiotic omission; (4) Outlining how to counsel patients who are treated without antibiotics; (5) Reviewing methods to safely implement this practice in both the hospital and community setting. These topics were divided up among members of the task force who performed a structured literature search in preparation for their assignments.

Antibiotics are associated with several patient and societal adverse effects, including the rising problem of antimicrobial resistance. Randomized controlled trials have demonstrated no superiority to the routine administration of antibiotics in acute uncomplicated diverticulitis. Appropriate patients for antibiotic omission include those who are immunocompetent, non-septic, and have mild symptoms/disease severity on imaging. Existing frameworks for the safe implementation of new practices can be referenced to help increase adoption of non-antibiotic therapy.

The existing body of evidence supports antibiotic omission in appropriate cases of acute uncomplicated diverticulitis. In order to increase the widespread adoption of this practice, buy-in from key stakeholders (both healthcare professionals and patients) is necessary.

Hypervirulent Klebsiella pneumoniae (hvKp) strains are increasingly recognized for their aggressive nature, which leads to severe clinical outcomes. The emergence of multidrug-resistant strains constitutes a substantial challenge for clinical management. Phage therapy offers a potential solution to the antibiotic resistance crisis. A multidrug-resistant hvKp strain, K2420 (K20 serotype), was used to isolate bacteriophages from hospital sewage. Phage morphology, biological properties, and genome characteristics were analyzed using transmission electron microscopy, plaque assays, and whole-genome sequencing. Therapeutic safety and efficacy were assessed in an acute pneumonia murine model induced by intratracheal injection of K2420. Assessment parameters included bacterial load, phage titer, body temperature, cytokine levels, histopathological findings, and other relevant indicators. Phage PK2420, a member of the Autographiviridae family and Przondovirus genus, was identified. It rapidly lyses K. pneumoniae (K20 serotype), inhibits biofilm formation, and exhibits a burst size of 37.4 plaque-forming units/cell. The phage is stable at temperatures ranging from 0°C to 40°C and pH values between 6 and 9. Its genome, 41,155 bp in length, contains 46 coding sequences. The phage has no genes associated with antibiotic resistance, virulence, or lysogeny. In vivo, PK2420 substantially reduced K. pneumoniae bacterial loads, improved survival rates, and alleviated pneumonia severity without observable side effects. Phage PK2420 exhibits lytic activity against K. pneumoniae both in vitro and in murine models, providing a promising and safe option for the treatment of hvKp infections.IMPORTANCEOur investigation provides insights into the interaction mechanism among hypervirulent Klebsiella pneumoniae (hvKp) (K20 serotype), phage, and the host in a mouse pneumonia model, offering a valuable reference for future research on phage pharmacokinetics. This study demonstrated that bacteriophage PK2420 exhibits promising biosafety and therapeutic efficacy against hvKp-induced pulmonary infections and dissemination in a murine model. These findings suggest that phage PK2420 may be a potential option for the clinical treatment of hvKp infections.

Epilepsy, a widespread chronic neurological disorder, has recently come under scrutiny for its potential association with the intricate dynamics of gut microbiota. Numerous investigations into the microbiota-gut-brain axis have revealed a close relationship between gut microbiota and epilepsy, suggesting gut microbiota as a potential treatment strategy. In clinical practice, a longstanding correlation has been observed between some kinds of antibiotics and the potential to induce seizures. Consequently, we have conceived a hypothesis that antibiotics might impact seizure activity by modulating the gut microbiota and influencing the physiological processes within the microbiota-gut-brain axis. In this review, our primary objective is to present the existing evidence and theoretical foundations supporting the hypothesis that dysbiosis within the gut microbiota may play a significant role in the pathophysiology of epilepsy. Furthermore, we aim to summarize the possible mechanisms between microbiota-gut-brain axis and epilepsy, offering insights into the selection of appropriate antibiotics for long-term epilepsy management and enhancing therapeutic efficacy through modulation of the gut microbiota. Further research is necessary to fully elucidate the intricate relationship between gut microbiota ecosystem and epilepsy. Exploring these connections holds promise for advancing our understanding of epilepsy pathogenesis and improving patient treatment and care.

Bile acids, derived from cholesterol in the liver, consist a steroidal core. Primary bile acids and secondary bile acids metabolized by the gut microbiota make up the bile acid pool, which modulate nuclear hormone receptors to regulate immunity. Disruptions in the crosstalk between bile acids and the gut flora are intimately associated with the development and course of gastrointestinal inflammation.

This review provides an extensive summary of bile acid production, transport and metabolism. It also delves into the impact of bile acid metabolism on the body and explores the involvement of bile acid-microbiota interactions in various disease states. Furthermore, the potential of targeting bile acid signaling as a means to prevent and treat inflammatory bowel disease is proposed.

In this review, we primarily address the functions of bile acid-microbiota crosstalk in diseases. Firstly, we summarize bile acid signalling and the factors influencing bile acid metabolism, with highlighting the immune function of microbially conjugated bile acids and the unique roles of different receptors. Subsequently, we emphasize the vital role of bile acids in maintaining a healthy gut microbiota and regulating the intestinal barrier function, energy metabolism and immunity. Finally, we explore differences of bile acid metabolism in different disease states, offering new perspectives on restoring the host's health and the gastrointestinal ecosystem by targeting the gut microbiota-bile acid-bile acid receptor axis.

A number of investigations have shown that gut microbiome influences humans' ability to communicate with others, and impairments in social interactions are linked to alterations in gut microbiome composition and diversity, via epigenetic mechanisms. This article reviews the links among gut microbiome, social behavior, and epigenetic shifts relevant to gut microbiome-derived metabolites. First, we discuss how different social determinants of health, such as socioeconomic status, diet, environmental chemicals, migration, ecological conditions, and seasonal changes may influence gut microbiome composition, diversity, and functionality, along with epigenetic alterations and thereby affect social behavior. Next, we consider how gut microbiome-derived metabolites, diet, probiotics, and fecal microbiome transplantation may reduce impairments in social interactions through the adjustment of epigenetic aberrations (e.g., DNA methylation, histone modifications, and microRNAs expression) which may suppress or increase gene expression patterns. Finally, we present the potential benefits and unresolved challenges with the use of gut microbiome-targeted therapeutics in reducing social deficits.

The initial microbial colonization of the gut is seeded by microbes transmitted from the mother's gut, skin, and vaginal tract. As the gut microbiome evolves, a few transmitted microbes persist throughout life. Understanding the impact of mother-to-neonate gut microbiome and antibiotic resistance genes (ARGs) transmission is crucial for establishing its role in infants' immunity against pathogens.

This study primarily explores mother-neonate ARG transmission through 125 publicly available fecal metagenomes, isolated from eighteen mother-neonate pairs.

The core ARGs, detected in both mothers and their respective infants at all stages (birth, 1st, 2nd, 3rd, 4th, 8th and 12th months) included aminoglycosidases APH(3')-IIIa, Bifidobacterium adolescentis rpoB mutants conferring resistance to rifampicin, β-lactamases CblA-1, CfxA2, multidrug resistance gene CRP, diaminopyrimidine resistance gene dfrF, fluoroquinolone-resistance gene emrR, macrolide; lincosamide; streptogramin resistance gene ErmB, ErmG, macrolide resistance gene Mef(En2), nucleosidase SAT-4, and tetracycline-resistance genes tet(O), tet(Q), and tet(W). Most of these infants and mothers were not administered any antibiotics. In infants, ARGs were predominantly carried by Bacillota, Pseudomonadota, and Actinomycetota, similar to the mothers. The dominant ARG-carrying opportunistic pathogens were Escherichia coli, Klebsiella, and Streptococcus, found across all infant cohorts. All the core ARGs were associated with mobile genetic elements, signifying the role of horizontal gene transfer(HGT). We detected 132 virulence determinants, mostly E. coli-specific, including pilus chaperones, general secretion pathway proteins, type III secretion system effectors, and heme-binding proteins.

Maternal-neonate transmission of ARGs along with possible nosocomial infections, mode of delivery, breastfeeding versus formula feeding, and gestation period, must be considered for mother-neonate health.

Antibiotics may disrupt the intestinal microbiota balance and induce antimicrobial resistance. Although probiotics should be a priority treatment for animal diarrhea, it still has chance to be used as same/or behind as antibiotics in the clinic. Among the probiotics, Lactobacillus (Lact.) was the most frequently utilized in clinical setting since its excellent ability of safety, anti-pathogen, stress resistance, and easy colonization in intestine. In this study, we screened 24 strains of Lact. in the presence of antibiotics from clinical common antibiotic-treated feces, identified L. salivarius LSbg3 exhibiting good stress resistance, potent antibacterial activity, and exceptional intestinal adhesion capability. Its genome showed a good function of regulating intestinal nutrition while lack of transmission antibiotic-resistance genes. Additionally, in a simulated canine diarrhea with failed antibiotic treatment, LSbg3 had a good efficacy in the releasing diarrhea, balancing the microbiome and suppressing typical pathogens, positioning a potential food probiotic have excellent effect on anti-pathogen that can effectively improve antibiotic-resistant diarrhea in dogs.

In recent years, chimeric antigen receptor (CAR)-T cell therapy has achieved tremendous efficacy in relapsed/refractory multiple myeloma (R/R MM). However, the impact of antibiotic (ATB) use on R/R MM patients treated with CAR-T is still not known. The aim of our study was to analyse the influence of ATB on the clinical outcomes of R/R MM patients treated with CAR-T cells.

In this retrospective study, 199 patients with R/R MM who received CAR-T cells between January 2018 and December 2023 were evaluated from two hospitals in China. They were stratified into ATB-group and No ATB-group according to whether ATB was administered in the 4 weeks before therapy. We mainly analyzed the efficacy, survival outcomes and cytotoxicity of CAR-T cell therapy in two groups of patients.

In the ATB group (90 patients), the overall response rate (ORR) was 70% comparable to the No ATB group (109 patients: ORR, 81.7%; P = 0.054). The complete response rate (CRR) was 40%, which was significantly lower compared with No ATB group (CRR, 57.8%; P = 0.012). The median progression-free survival (PFS) was 6.7 months while the median overall survival (OS) was 21.9 months for the ATB group. The median PFS and OS for the No ATB group were 13.9 months and 36.1 months. There were significant differences in PFS (P = 0.007) and OS (P = 0.004) between the evaluated groups. Nonetheless, multivariate analysis found ATB use did not reduce the CRR (odds ratio [OR], 0.947; 95% confidence interval [CI], 0.251 to 3.565, P = 0.936). Besides, administration of ATB did not affect the PFS (hazard ratio [HR], 0.634; 95% CI, 0.28 to 1.436, P = 0.275) and OS (HR, 2.259; 95% CI, 0.755 to 6.762, P = 0.145) in R/R MM patients treated with CAR-T cells. Additionally, both groups of patients had similar incidences of cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS).

Our results point to a detrimental effect of ATB on treatment outcomes to CAR-T cell therapy. However, the use of ATB is not associated with the incidence of CRS or ICANS.

The PROGRESS randomised trial (ClinicalTrials.gov: NCT03333304) showed that early stopof antibiotics guided by procalcitonin (PCT) decreased the incidence of infections by multidrug-resistant organisms and/or Clostridioides difficile and was associated with survival benefit. This study was conducted to investigate whether this survival benefit is associated with microbiome dysbiosis. Patients with sepsis due to lung infection, acute pyelonephritis or primary bacteraemia were randomised to standard-of-care (SoC) duration of antibiotics or early stop using PCT. Faecal samples were collected before, and 7 and 28 days after randomisation and analysed using 16S rRNA Nanopore sequencing. Calprotectin was measured using an enzyme immunoassay. Median (Q1-Q3) antimicrobial duration was 5 (5-7.5) days in the PCT arm and 11 (8-15) days in the SoC arm (P < 0.001). Faecal calprotectin levels were similar in the two treatment arms at baseline. By day 7, the levels of faecal calprotectin were significantly increased in the SoC arm (P = 0.002) but were unchanged in the PCT arm. Microbiome α- and β-diversity was similar at baseline in the PCT (n=81) and SoC (n=76) treatment arms. Shannon's index was significantly lower in the SoC arm on day 7 compared with baseline (median [Q1-Q3], 2.88 [2.37-3.39] at day 1 vs. 2.24 [1.52-3.08] at day 7; Pt-test = 0.0013). This was not the case for the PCT arm (median [Q1-Q3], 2.73 [2.26-3.4] at day 1 vs. 2.43 [1.81-3.21] at day 7; Pt-test = 0.037, Bonferroni corrected α = 0.0125). The relative abundance of Actinomycetota and Pseudomonadota was decreased in the PCT arm by day 7 and that of Bacillota was increased. Early PCT-guided stop of antibiotics contributes to decreased microbiome dysbiosis by day 7.

The microbiota-gut-brain axis has been proposed as a potential modulator of mood disorders such as major depression. Complex bidirectional biochemical activities in this axis have been posited to participate in adverse mood disorders. Environmental and genetic factors have dominated recent discussions on depression. The prescription of antibiotics, antidepressants, adverse negative DNA methylation reactions and a dysbiotic gut microbiome have been cited as causal for the development and progression of depression. While research continues to investigate the microbiome-gut-brain axis, this review will explore the state of persistence of gut bacteria that underpins bacterial dormancy, possibly due to adverse environmental conditions and/or pharmaceutical prescriptions. Bacterial dormancy persistence in the intestinal microbial cohort could affect the role of bacterial epigenomes and DNA methylations. DNA methylations are highly motif driven exerting significant control on bacterial phenotypes that can disrupt bacterial metabolism and neurotransmitter formation in the gut, outcomes that can support adverse mood dispositions.

Antibiotics, which have been identified as emerged pollutants, are creating an increase in environmental concerns, with sulfonamide antibiotics (SAs) being among the most commonly discovered antibiotics. Due to their widespread usage and inadequate sewage treatment, SAs are frequently released into the aquatic environment. The introduction of SAs into aquatic environments can kill or inhibit the growth or metabolic activity of microorganisms, thereby affecting biological communities and ecological functions and disrupting the equilibrium of aquatic ecosystems. The transmission of SAs to human beings can occur through trophic transfer of food chains, particularly when humans consume aquatic food. This study examines the trophic transfer of SAs along the aquatic food chain, provides a summarize of the spatial distribution of SAs in aquatic environments, and evaluates the environmental risks associated with it. The prevalence of SAs was predominantly noted in the aqueous phase, with relatively lower concentrations detected in sediments, solidifying their status as one of the most widespread antibiotics among aquatic organisms. SAs, characterized by their high biomagnification capacity and strong bioaccumulative properties in invertebrates, emerge as the antibiotic type with the greatest ecological risks. The ecological risk posed by sulfonamide antibiotics to aquatic organisms is more pronounced than the health risk to humans, suggesting that the adverse effects on aquatic life warrant greater attention. Additionally, this study offers practical recommendations to address the limitations of previous research, emphasizing the importance of regulating exposure and establishing a robust health risk prediction system as effective measures for antibiotic control.

The healthy gut microbiome is important in maintaining health and preventing various chronic and metabolic diseases through interactions with the host via different gut-organ axes, such as the gut-brain, gut-liver, gut-immune, and gut-lung axes. The human gut microbiome is relatively stable, yet can be influenced by numerous factors, such as diet, infections, chronic diseases, and medications which may disrupt its composition and function. Therefore, microbial resilience is suggested as one of the key characteristics of a healthy gut microbiome in humans. However, our understanding of its definition and indicators remains unclear due to insufficient experimental data. Here, we review the impact of key drivers including intrinsic and extrinsic factors such as diet and antibiotics on the human gut microbiome. Additionally, we discuss the concept of a resilient gut microbiome and highlight potential biomarkers including diversity indices and some bacterial taxa as recovery-associated bacteria, resistance genes, antimicrobial peptides, and functional flexibility. These biomarkers can facilitate the identification and prediction of healthy and resilient microbiomes, particularly in precision medicine, through diagnostic tools or machine learning approaches especially after antimicrobial medications that may cause stable dysbiosis. Furthermore, we review current nutrition intervention strategies to maximize microbial resilience, the challenges in investigating microbiome resilience, and future directions in this field of research.

Immunotherapy using immune checkpoint inhibitors (ICIs) has shown several benefits over traditional therapies. However, the eligible population remains small. Antibiotic (ATB) use might reduce immunotherapy efficacy by disrupting the gut microbiota. However, in China, ATB effect on ICI therapy efficacy remains unelucidated. We aimed to assess the effects of ATBs on the anti-tumor efficacy of ICIs to provide a reference for clinical use.

We included 134 patients with advanced tumors undergoing ICI therapy at Shanghai Jiading District Central Hospital from January 1, 2021, to October 1, 2023. They were divided into Non-ATB and ATB groups based on ATB use within 30 days before and after ICI administration. Moreover, we compared progression-free (PFS) and overall (OS) survival between the groups.

Median PFS and OS were lower in the ATB than in the Non-ATB group (PFS: 4.0 vs. 5.5 months; OS: 5.4 vs. 6.5 months). Univariate analysis revealed that ATB use significantly affected PFS (hazard ratio [HR] = 2.318, 95% confidence interval [CI] = 1.281-4.194, P = 0.005) and OS (HR = 2.115, 95% CI = 1.161-3.850, P = 0.014). Moreover, multivariate analysis revealed poor PFS (HR = 2.573, 95% CI = 1.373-4.826, P = 0.003) and OS (HR = 2.452, 95% CI = 1.298-4.632, P = 0.006) in patients who received ATBs during ICI therapy.

ATB use is negatively correlated with ICI therapy efficacy, leading to reduced PFS and OS in patients undergoing such treatment. Owing to the significant impact of ATBs on the human gut microbiome, regulation of the gut microbiome may emerge as a novel therapeutic target that can enhance the clinical activity of ICIs.

Available evidence illustrates that microbiome is a promising target for the study of growth, diagnosis and therapy of various types of cancer. Lung cancer is a leading cause of cancer death worldwide. The relationship of microbiota and their products with diverse pathologic conditions has been getting large attention. The novel research suggests that the microbiome plays an important role in the growth and progression of lung cancer. The lung microbiome plays a crucial role in maintaining mucosal immunity and synchronizing the stability between tolerance and inflammation. Alteration in microbiome is identified as a critical player in the progression of lung cancer and negatively impacts the patient. Studies suggest that healthy microbiome is essential for effective therapy. Various clinical trials and research are focusing on enhancing the treatment efficacy by altering the microbiome. The regulation of microbiota will provide innovative and promising treatment strategies for the maintenance of host homeostasis and the prevention of lung cancer in lung cancer patients. In the current review article, we presented the latest progress about the involvement of microbiome in the growth and diagnosis of lung cancer. Furthermore, we also assessed the therapeutic status of the microbiome for the management and treatment of lung cancer.

Oral antibiotic treatment is well known to be one of the main factors affecting gut microbiota composition by altering bacterial diversity. It decreases the abundance of butyrate-producing bacteria such as Lachnospiraceae and Ruminococcaceae, while increasing abundance of Enterobacteriaceae. The recovery time of commensal bacteria post-antibiotic treatment varies among individuals, and often, complete recovery is not achieved. Recently, gut microbiota disruption has been associated with increased gut oxygen levels and higher redox potential in faecal samples. Given that redox balance is crucial for microbial metabolism and gut health, influencing fermentation processes and maintaining anaerobic conditions, we investigated the impact of oral amoxicillin treatment on the redox potential in the caecum. We used 24 Wistar Han male rats and measured caecal redox potential in situ with a probe, before and after 7 days of amoxicillin treatment, as well as after 7 days of recovery. Additionally, we analysed caecal weight, pH, antioxidant capacity, caecal microbiota, metabolome, and colonic tissue expression of relevant genes involved in the redox potential state. Our findings show that oral amoxicillin treatment significantly reduced archaeal load, and decreased the bacterial alpha diversity and affected bacterial composition of the caecal microbiome. The caecal metabolome was also significantly affected, exemplified by reduced amounts of short chain fatty acids during amoxicillin treatment. While the caecal metabolome fully recovered 7 days post amoxicillin treatment, the microbiome did not fully recover within this time frame. However, amoxicillin did not lead to an increase in luminal redox potential in the cecum during or post amoxicillin treatment. Limited differences were observed for colonic expression of genes involved in intestinal barrier function and generation of reactive oxygen species, except for the catalase gene, which was significantly upregulated post-amoxicillin treatment. Our results suggest that while oral amoxicillin disrupts the gut microbiome and metabolome, it does not directly interfere with gut luminal redox state.

It is important to promote intestinal development and maturation of chicks for feed digestion and utilization, intestinal health, and disease resistance. This study aimed to investigate the effects of dietary yeast cell wall polysaccharides (YCWP) addition on intestinal development and maturation of chickens and its potential action mechanism.

180 one-day-old male Arbor Acres broilers were randomly assigned to three groups containing control (basal diets without any antibiotics or anticoccidial drug), bacitracin methylene disalicylate (BMD)-treated group (50 mg/kg) and YCWP-supplemented group (100 mg/kg).

Compared with control group, in-feed antibiotic BMD continuous administration significantly decreased crypt depth (d 21) and villus height (d 42) along with mucosal maltase activity (d 42) in the ileum (P < 0.05). Also, BMD markedly downregulated gene expression levels of β-catenin, lysozyme, occludin and FABP-2 (d 21) and innate immune related genes CD83 and MHC-I mRNA levels (d 42, P < 0.05), and decreased goblet cell counts in the ileum of chickens (d 21 and d 42, P < 0.05). While, TLR-2, TLR-6 and iNOS mRNA abundances were notably upregulated by BMD treatment (d 42, P < 0.05). Nevertheless, dietary YCWP addition significantly increased the ratio of villus height to crypt depth (d 21), villus surface area (d 21 and d 42), ileal alkaline phosphatase and maltase activities as well as goblet cell (d 21 and d 42) and IgA-producing plasma cell numbers as compared to BMD treatment (d 21, P < 0.05). YCWP addition also upregulated gene expression levels of Lgr5, Wnt/β-catenin signaling pathway related gene (Wnt3, β-catenin, d 21; β-catenin, d 42), intestinal cells proliferation marker Ki-67 and barrier function related genes (occludin, d 21 and d 42, P < 0.05). Moreover, YCWP significantly increased antigen presenting cell marker related genes (MHC-II, d 21; CD83 and MHC-I, d 42), TLR-1, TLR-2 and TLR-6 mRNA levels (d 21, P < 0.05). Cecal microbiome analysis showed that YCWP addition obviously improved cecal microbial composition, as indicated by increasing relative abundance of Fournierella, Psychrobacter and Ruminiclostridium on d 21, and Alistipes and Lactobacillus on d 42, which were positively related with gut development and maturation related indexes (P < 0.05).

Collectively, YCWP promoted yet antibiotic BMD delayed intestinal morphological and immunological development linked with modulating gut microbiome in chickens.

Antibiotic overuse is driving a global rise in antibiotic resistance, highlighting the need for robust antimicrobial stewardship (AMS) initiatives to improve prescription practices. While antimicrobials are essential for treating sepsis and preventing surgical site infections (SSIs), they can inadvertently disrupt the gut microbiota, leading to postoperative complications. Treatment methods vary widely across nations due to differences in drug choice, dosage, and therapy duration, affecting antibiotic resistance rates, which can reach up to 51% in some countries. In Romania and the Republic of Moldova, healthcare practices for surgical antibiotic prophylaxis differ significantly despite similarities in genetics, culture, and diet. Romania's stricter healthcare regulations result in more standardized antibiotic protocols, whereas Moldova's limited healthcare funding leads to less consistent practices and greater variability in treatment outcomes.

This study presents the results of a prospective cross-border investigation involving 86 colorectal cancer patients from major oncological hospitals in Romania and Moldova. We analyzed fecal samples collected from patients before and 7 days post-antibiotic treatment, focusing on the V3-V4 region of the 16S rRNA gene.

Our findings indicate that inconsistent antibiotic prophylaxis policies-varying in type, dosage, or therapy duration-significantly impacted the gut microbiota and led to more frequent dysbiosis compared to stricter prophylactic antibiotic practices (single dose, single product, limited time).

We emphasize the need for standardized antibiotic prophylaxis protocols to minimize dysbiosis and its associated risks, promoting more effective antimicrobial use, particularly in low- and middle-income countries (LMICs).

Human microbiota is noteworthy for its ability to encode a much greater variety and quantity of proteins than human cells. Despite its dynamic and complex nature, it has been associated with healthy living for over a century. The knowledge and attitudes of healthcare professionals, especially physicians, influence the use of pro-prebiotic interventions to modulate the microbiota. This study aimed to examine the awareness of medical students about the microbiota and the factors influencing their awareness.

The study was conducted between May 15 and August 15, 2023, with the participation of 235 medical students. The students were administered a 13-item questionnaire and the Microbiota Awareness Scale (MAS). The questionnaire and scale were administered face-to-face, and the results were statistically analyzed.

The students' MAS total mean score was 70.34 ± 8.15. The MAS scores of medical students in the 4th, 5th, and 6th grades who underwent clinical training, those who conducted research on microbiota independently, those who had previously used prebiotics/probiotics, and those who rated themselves highly on microbiota knowledge were statistically higher.

The study revealed that students' awareness of the microbiota increased with advancing years of medical education, reaching a high level by the time of graduation. To enable future physicians to effectively communicate this knowledge to the public and incorporate it into clinical practice, it is crucial to provide comprehensive education on microbiota, probiotics, and prebiotics during medical training. Additionally, promoting scientific research and organizing activities in these areas are essential for fostering deeper understanding and practical application.

Antibiotics are the most commonly prescribed drugs during pregnancy. The long-term health risks to children associated with prenatal antibiotic exposure are uncertain.

To identify the association between prenatal antibiotics and adverse long-term health outcomes in children.

A systematic search was done to identify original studies investigating the association between prenatal antibiotic exposure and adverse long-term health outcomes in children. Studies were excluded if: (i) antibiotics were only given during delivery or (ii) the outcome was present before antibiotic exposure.

We included 158 studies, reporting 23 outcomes in 21,943,763 children, in our analysis. For the following adverse health outcomes, there was a significant association with antibiotic exposure found in two or more studies: atopic dermatitis (OR 1.27, 95% CI 1.06-1.52, p=0.01), food allergies (OR 1.25, 95% CI 1.09-1.44, p<0.01), allergic rhinoconjunctivitis (OR 1.16, 95% CI 1.15-1.17, p<0.01), wheezing (OR 1.39, 95% CI 1.14-1.69, p<0.01), asthma (OR 1.36, 95% CI 1.24-1.50, p<0.01), obesity (OR 1.36, 95% CI 1.12-1.64, p<0.01), cerebral palsy (OR 1.25, 95% CI 1.10-1.43, p<0.01), epilepsy or febrile seizure (OR 1.16, 95% CI 1.08-1.24, p<0.01), and cancer (OR 1.13, 95% CI 1.01-1.26, p=0.04).

Although causality cannot be implied, these findings support antibiotic stewardship efforts to ensure judicious use of antibiotics during pregnancy to avoid potential long-term health risks.

Clostridium perfringens (C. perfringens) type C exhibits strong pathogenicity, often leading to swine dysentery, severely affecting the economic efficiency of the pig farming industry. Bacteriophages as bacterial viruses have many natural advantages and are potent candidates for controlling bacterial infections. In this study, a lytic C. perfringens phage designed as vB_CpeP_15N3 was isolated with the host C. perfringens type C CVCC1155, and its potential for therapy was determined in vitro and in vivo. Despite the narrow host range, phage vB_CpeP_15N3 exhibited a large burst size of 102 PFU/cell following a short latent period of 10 min. In addition, phage vB_CpeP_15N3 remained stable at temperatures ranging from 4 to 50°C and pH levels from 5 to 9 and had a strong antibacterial effect in vitro. Through whole-genome analysis, phage vB_CpeP_15N3 belongs to the family Guelinviridae, genus Brucesealvirus with no genes related to lysogeny and bacterial virulence or resistance. We further demonstrated that phage vB_CpeP_15N3 by oral administration for preventive purposes could significantly alleviate clinical symptoms and jejunal lesions of newborn piglets through the reduced colonization of C. perfringens type C in the jejunum and the level of CPB toxin in the content of jejunum in the newborn piglet model of CVCC1155 infection. In addition, phage vB_CpeP_15N3 by oral administration for preventive purposes could improve the diversity and abundance of the jejunum microbiota in newborn piglets. Moreover, the prevention by phage vB_CpeP_15N3 obtained more effective therapeutic results than phage and gentamicin treatments. Taken together, these findings suggested that phage vB_CpeP_15N3 is a promising alternative of antibiotics for preventing and controlling C. perfringens type C infection of newborn piglets.

Ciprofloxacin is an antibiotic from the fluoroquinolone group that is frequently used in many clinical practices. In addition to its peripheral neuropathic side effects, it is an antibiotic that can pass through the blood-brain barrier due to its lipophilic features and cause rare central nervous system symptoms. Although cases of neuropsychiatric symptoms developing after treatment with ciprofloxacin have been reported in the literature, the number of reports of manic episodes after ciprofloxacin use is limited, and there have been no reports of delirious mania developing after ciprofloxacin use until the case presented in this report. Here we report the case of a 52-year-old woman who developed manic symptoms after receiving ciprofloxacin, which evolved into delirious mania. Clinical factors that may predispose to neurotoxicity are discussed and compared with features of the mania cases in the literature. The underlying neurobiological mechanisms are also reviewed.

Introduction. Type 2 diabetes mellitus (T2DM) is a major global health issue projected to exceed 700 million cases by 2045. In Malaysia, T2DM prevalence has risen, with notable ethnic disparities.Gap statement. The gut microbiota's role in T2DM pathogenesis is well recognized, yet its composition in Malaysia's ethnically diverse population remains underexplored.Aim. This study aimed to characterize gut microbiota composition among T2DM and ethnicity-matched adults without diabetes (nonDM) in Malaysia.Methodology. A case-control study was conducted with 45 T2DM and 45 nonDM participants matched by ethnicity from a primary care clinic in Klang Valley, Malaysia. Faecal DNA was subjected to 16S rRNA sequencing to identify microbiota diversity and composition differences and compare predicted functional capabilities. Correlations between bacterial taxa, clinical characteristics and dietary intake were analysed.Results. T2DM participants showed decreased alpha diversity (observed, P-value=0.002, r=0.69; Shannon, P-value<0.001, r=0.73) and significant differences in beta diversity (permutational multivariate ANOVA, R²=0.036, P-value=0.001). Linear discriminant analysis effect size and multiple regression analysis, adjusted for covariates age, gender, BMI and intakes of protein, fat, carbohydrate and fibre, identified the phylum Proteobacteria and genera Escherichia-Shigella to be increased, while the genera Anaerostipes and Romboutsia decreased in T2DM. These bacteria were associated with various clinical characteristics and dietary intake. However, these 'potential biomarkers' were not uniformly present across all participants, suggesting that individual bacterial taxa may not serve as universal biomarkers.Conclusion. Significant gut microbiota differences exist between T2DM and nonDM individuals in Malaysia, indicating a dysbiosis characterized by increased pro-inflammatory bacteria and reduced short-chain fatty acid-producing bacteria in T2DM. While these findings highlight the potential functional relevance of gut microbiota in T2DM pathogenesis, addressing limitations such as participant matching for confounding factors in future studies could uncover additional significant differences in microbiota composition. Furthermore, the variability in taxa prevalence across individuals suggests that targeting microbial metabolic products may offer more promising strategies to inform microbiota-targeted interventions than relying solely on specific bacterial taxa as biomarkers.

Intestinal inflammation is a common and serious health problem in piglet production, especially enteritis caused by pathogenic Escherichia coli (E. coli). This condition often leads to high mortality, slow weight gain, and significant economic losses.

In this study, we isolated an E. coli strain, SKLAN202302, from the colon of diarrheal piglets to create an intestinal inflammation model for evaluating the protective effects of baicalin. Piglets infected with E. coli exhibited significant reductions in body weight, feed intake, small intestine length, and ileal goblet cell count (P < 0.05), along with deteriorated ileal morphology. However, baicalin supplementation resulted in body weights, feed intake, and intestinal morphology similar to those of the control group. Notably, there was a significant increase in the colonization of Lactobacillus species, particularly Lactobacillus_reuteri, Lactobacillus_amylovorus, and Lactobacillus_johnii, compared to the E. coli group (P < 0.05). At the metabolic and transcriptional levels, E. coli infection increased inflammatory mediators, including eicosanoids (leukotriene F4, prostaglandin F1a, leukotriene E4, thromboxane B2, prostaglandin G2, and PGH2), monosaccharides, and TCA cycle intermediates (oxoglutaric acid, glutaric acid, adipic acid, citric acid, and isocitric acid) in the ileum. It also promoted the expression of genes related to autoimmune diseases and the Th17 differentiation signaling pathway (CTLA4, IFN-ALPHA-8, IL12RB2, TRAV3, TRAV16, FOS, and VEGFA), as well as inflammatory factors. Conversely, baicalin supplementation not only counteracted these effects but also enhanced the presence of metabolites such as phospholipids [including lysoPC (P-18:1(9Z)/0:0), PC (17:0/0:0), lysoPC (16:1(9Z)/0:0), PC (18:0/0:0), lysoPC (18:0/0:0), PA (10:0/i-16:0), and PA (10:0/8:0)] and amino acids. It also regulated genes within the IL-17 signaling pathway (IL4, CCL17, CXCL10, IFNG, and CXCL2), suggesting a mechanism by which baicalin mitigates E. coli-induced intestinal and microbial disturbances. Subsequent flow cytometry analysis showed that E. coli infection increased the numbers of CD3+ and Foxp3+ cells, decreased IL-17A+ cells, and reduced Th17/Treg ratios. Baicalin supplementation restored these parameters to control levels.

Baicalin supplementation effectively alleviates E. coli-induced intestinal inflammation and microbial disturbances in piglets by enhancing beneficial Lactobacillus colonization, counteracting inflammatory mediators, and regulating immune-related gene expression and the Th17/Treg balance. These findings highlight baicalin's potential in alleviating intestinal inflammation.

The intestinal microbiota plays a critical role in host immunity and might contribute to the significant variation between individuals' vaccine responses. A systematic search was done using MEDLINE and Embase to identify original human studies investigating the association between intestinal microbiota composition and humoral and cellular vaccine responses. In total, 30 publications (26 studies, 14 in infants, 12 in adults), were included. Of these, 26 publications found an association between intestinal microbiota composition and vaccine responses. A beneficial effect of Actynomycetota (particularly Bifidobacterium) and a detrimental effect of Pseudomonadota (particularly Gammaproteobacteria) were observed across studies. Study designs were highly heterogenous, with variation in vaccine type, outcome measure, timing of stool analysis and analysis methods. Overall, studies support the concept that the composition of the intestinal microbiota influences vaccine responses. Further adequately powered studies are needed to confirm this association and inform potential microbiota-targeted interventions to optimise vaccine responses.

Sepsis is a life-threatening complication caused by an uncontrolled immune response to infection that can lead to multi-organ dysfunction, including liver injury. Recent research has shown the critical role of gut microbiota in sepsis pathogenesis, with the gut-liver axis playing a crucial role in disease progression. Mechanisms such as the disruption of the gut barrier and liver injury pathways mediated by cytokines, chemokines, adhesion molecules, hydrogen sulfide (H2S). and substance P (SP) have been the focus of recent studies. Some potential biomarkers and gut microbiota-targeted therapies have shown promise as emerging tools for predicting and managing sepsis. This review describes the role of the gut-liver axis in sepsis and the potential of microbiota-targeted therapies and biomarker-driven interventions to improve sepsis outcomes.

Antibiotics, widely used medications that have significantly increased life expectancy, possess a broad range of effects beyond their primary antibacterial activity. While some are recognized as adverse events, others have demonstrated unexpected benefits. These adjunctive effects, which have been defined as "pleiotropic" in the case of other pharmacological classes, include immunomodulatory properties and the modulation of the microbiota. Specifically, macrolides, tetracyclines, and fluoroquinolones have been shown to modulate the immune system in both acute and chronic conditions, including autoimmune disorders (e.g., rheumatoid arthritis, spondyloarthritis) and chronic inflammatory pulmonary diseases (e.g., asthma, chronic obstructive pulmonary disease). Azithromycin, in particular, is recommended for the long-term treatment of chronic inflammatory pulmonary diseases due to its well-established immunomodulatory effects. Furthermore, antibiotics influence the human microbiota. Rifaximin, for example, exerts a eubiotic effect that enhances the balance between the gut microbiota and the host immune cells and epithelial cells. These pleiotropic effects offer new therapeutic opportunities by interacting with human cells, signaling molecules, and bacteria involved in non-infectious diseases like spondyloarthritis and inflammatory bowel diseases. The aim of this review is to explore the pleiotropic potential of antibiotics, from molecular and cellular evidence to their clinical application, in order to optimize their use. Understanding these effects is essential to ensure careful use, particularly in consideration of the threat of antimicrobial resistance.

Leukemia poses significant challenges to its treatment, and understanding its complex pathogenesis is crucial. This study used metagenomic sequencing to investigate the interplay between chemotherapy, gut microbiota, and antibiotic resistance in patients with acute leukemia (AL). Pre- and post-chemotherapy stool samples from patients revealed alterations in microbial richness, taxa, and antibiotic resistance genes (ARGs). The analysis revealed a decreased alpha diversity, increased dispersion in post-chemotherapy samples, and changes in the abundance of specific bacteria. Key bacteria such as Enterococcus, Klebsiella, and Escherichia coli have been identified as prevalent ARG carriers. Correlation analysis between gut microbiota and blood indicators revealed potential links between microbial species and inflammatory biomarkers, including C-reactive protein (CRP) and adenosine deaminase (ADA). This study investigated the impact of antibiotic dosage on microbiota and ARGs, revealing networks connecting co-occurring ARGs with microbial species (179 nodes, 206 edges), and networks associated with ARGs and antibiotic dosages (50 nodes, 50 edges). Antibiotics such as cephamycin and sulfonamide led to multidrug-resistant Klebsiella colonization. Our analyses revealed distinct microbial profiles with Salmonella enterica elevated post-chemotherapy in NF patients and Akkermansia muciniphila elevated pre-chemotherapy. These microbial signatures could inform strategies to modulate the gut microbiome, potentially mitigating the risk of neutropenic fever in patients undergoing chemotherapy. Finally, a comprehensive analysis of KEGG modules shed light on disrupted metabolic pathways after chemotherapy, providing insights into potential targets for managing side effects. Overall, this study revealed intricate relationships between gut microbiota, chemotherapy, and antibiotic resistance, providing new insights into improving therapy and enhancing patient outcomes.

Cefmetazole (CMZ) is a carbapenem-sparing option in the treatment of extended-spectrum beta-lactamase (ESBL)-producing bacterial infection. In this pilot study, we aimed to compare the effects of antimicrobial treatment (meropenem [MP] and CMZ) with those of no antimicrobial treatment (control group) on the microbiome.

The study was a multicenter, prospective, observational pilot study conducted from October 2020 to October 2022. Feces and saliva samples were collected for microbiome analyses at two time points (early-period: days 1-3; and late-period: days 4-30) for the antimicrobial treatment group, and at one time point for the control group.

Five feces (MP-F and CMZ-F) and five saliva (MP-S and CMZ-S) samples were included in the MP and the CMZ groups. Ten feces (C-F) and saliva (C-S) samples were included in the control group. Group α diversity was notably lower in the late-period MP-F group than the control group as determined with the Shannon richness index. β diversity analysis of the feces samples based on weighted and unweighted UniFrac distances revealed distinctions in both the late-period CMZ-F and MP-F groups compared with the control group. Weighted UniFrac analysis showed that only the early-period MP-F group differed from the control group. In the saliva samples, weighted and unweighted UniFrac analyses showed significant differences between the control group and the early CMZ, late CMZ, and late MP groups.

MP treatment may cause larger impact on the feces microbiome than CMZ in Japanese patients.

This study aimed to evaluate the impact of antibiotic exposure on efficacy and adverse reactions in non-small cell lung cancer (NSCLC) patients receiving chemoimmunotherapy, and to explore any specific associations on the basis of antibiotic class.

A retrospective study was conducted on NSCLC patients who received chemoimmunotherapy in two Shandong hospitals between January 2018 and October 2023. The association between antibiotic exposure and progression-free survival (PFS), overall survival (OS), objective response rate (ORR) and incidence of immune related adverse reactions (irAE) of patients were evaluated.

Of the 316 patients, 134 (42.41%) received antibiotics (ATB group), and 182 (57.59%) did not (N-ATB group). There was no significant difference in PFS (aHR = 1.009, 95% CI: 0.770-1.323; p = 0.946) or OS (aHR = 1.420, 95% CI: 0.986-2.047; p = 0.060) between ATB and N-ATB groups. The impact on efficacy was related to the type of antibiotic. β-Lactams (aHR = 1.737, 95% CI: 1.148-2.629; p = 0.009), in particular β-lactam/β-lactamase inhibitor combinations (BLBLIs) (aHR = 1.885, 95% CI: 1.207-2.944, p = 0.005) were associated with poorer OS. However, quinolones (aHR = 1.192, 95% CI: 0.861-1.650; p = 0.291) were not associated with OS. The incidence of irAEs was not significantly different between ATB and N-ATB groups (p = 0.073), but was higher with BLBLIs (p = 0.013).

In NSCLC patients receiving chemoimmunotherapy, no significant difference was observed in efficacy and incidence of irAEs between the ATB and the n-ATB groups. In antibiotic class analysis, β-lactams and specifically BLBLIs were observed to be associated with worse OS.

Rising rates of antibiotic resistance in uropathogenic bacteria compromise patient outcomes and prolong hospital stays. Consequently, new strategies are needed to prevent and control the spread of antibiotic resistance in uropathogenic bacteria. Over the past two decades, sizeable clinical efforts and research advances have changed urinary tract infection (UTI) treatment and prevention strategies to conserve antibiotic use. The emergence of antimicrobial stewardship, policies from national societies, and the development of new antimicrobials have shaped modern UTI practices. Future UTI management practices could be driven by the evolution of antimicrobial stewardship, improved and readily available diagnostics, and an improved understanding of how the microbiome affects UTI. Forthcoming UTI treatment and prevention strategies could employ novel bactericidal compounds, combinations of new and classic antimicrobials that enhance bacterial killing, medications that prevent bacterial attachment to uroepithelial cells, repurposing drugs, and vaccines to curtail the rising rates of antibiotic resistance in uropathogenic bacteria and improve outcomes in people with UTI.

Early gut microbiota (GM) dysbiosis can affect a child's health and has been linked to the onset of pathologies later in life. Breast milk is recognized as a major driver of the structure and dynamics of an infant's GM. In addition to nutritious and prebiotic compounds, milk contains a microbiota that is shaped by several maternal factors, including gut microorganisms and medications. However, the impact of the latter on the milk microbiota is still largely unknown. Here, we investigated the effects of amoxicillin on the milk microbiota and GM of lactating Göttingen Minipigs sows, a promising model for studying medication transfer during lactation.

Three sows were given amoxicillin (7 mg/kg/day) for three weeks starting from the second week after farrowing. Fecal and milk samples were collected before and after treatment and profiled by 16S rRNA amplicon sequencing.

Göttingen Minipigs' milk microbiota showed similarities to that of humans and conventional sows, with minor compositional shifts after treatment. At the genus level, we observed a decrease in Staphylococcus and o_Bacteroidales;Other;Other, and an increasing trend in the abundance of Streptococcus, Stenotrophomonas, f_Rhodobacteraceae;Other, Proteiniclasticum, f_Propionibacteriaceae;Other and Gemella. In contrast, as expected, the GM was strongly affected by amoxicillin, even at the phylum level.

In addition to demonstrating the relevance of Göttingen Minipigs as a valid model for studying the impact of medications on maternal milk and GM, our findings suggest that the milk microbiota may be more stable during antibiotic treatment than the GM.

Antibiotics are safe, effective drugs and continue to save millions of lives and prevent long-term illness worldwide. A large body of epidemiological, interventional and experimental evidence shows that exposure to antibiotics has long-term negative effects on human health. We reviewed the literature data on the links between antibiotic exposure, gut dysbiosis, and chronic disease (notably with regard to the "developmental origins of health and disease" ("DOHaD") approach). Molecular biology studies show that the systemic administration of antibiotic to infants has a rapid onset but also often a long-lasting impact on the microbial composition of the gut. Along with other environmental factors (e.g., an unhealthy "Western" diet and sedentary behavior), antibiotics induce gut dysbiosis, which can be defined as the disruption of a previously stable, functionally complete microbiota. Gut dysbiosis many harmful long-term effects on health. Associations between early-life exposure to antibiotics have been reported for chronic diseases, including inflammatory bowel disease, celiac disease, some cancers, metabolic diseases (obesity and type 2 diabetes), allergic diseases, autoimmune disorders, atherosclerosis, arthritis, and neurodevelopmental, neurodegenerative and other neurological diseases. In mechanistic terms, gut dysbiosis influences chronic disease through direct effects on mucosal immune and inflammatory pathways, plus a wide array of direct or indirect effects of short-chain fatty acids, the enteric nervous system, peristaltic motility, the production of hormones and neurotransmitters, and the loss of intestinal barrier integrity (notably with leakage of the pro-inflammatory endotoxin lipopolysaccharide into the circulation). To mitigate dysbiosis, the administration of probiotics in patients with chronic disease is often (but not always) associated with positive effects on clinical markers (e.g., disease scores) and biomarkers of inflammation and immune activation. Meta-analyses are complicated by differences in probiotic composition, dose level, and treatment duration, and large, randomized, controlled clinical trials are lacking in many disease areas. In view of the critical importance of deciding whether or not to prescribe antibiotics (especially to children), we suggest that the DOHaD concept can be logically extended to "gastrointestinal origins of health and disease" ("GOHaD") or even "microbiotic origins of health and disease" ("MOHaD").

This study explores the effects of disinfectant and antibiotic exposure on gut health, focusing on gut microbiota balance and gut immune function. Our analysis indicates that disinfectants increase the proportion of Gram-positive bacteria, particularly increasing Staphylococcus levels, while antibiotics increase the proportion of Gram-negative bacteria, especially Bacteroides levels. These changes disrupt microbial harmony and affect the gut microbiome's functional capacity. Additionally, our research reveals that both disinfectants and antibiotics reduce colon length and cause mucosal damage. A significant finding is the downregulation of NLRC4, a key immune system regulator in the gut, accompanied by changes in immune factor expression. This interaction between chemical exposure and immune system dysfunction increases susceptibility to inflammatory bowel disease and other gut conditions. Given the importance of disinfectants in disease prevention, this study advocates for a balanced approach to their use, aiming to protect public health while minimizing adverse effects on the gut microbiome and immune function.

Disinfectants are extensively employed across various sectors, such as the food sector. Disinfectants are widely used in various sectors, including the food processing industry, animal husbandry, households, and pharmaceuticals. Their extensive application risks environmental contamination, impacting water and soil quality. However, the effect of disinfectant exposure on the gut microbiome and the immune function of animals remains a significant, unresolved issue with profound public health implications. This highlights the need for increased scrutiny and more regulated use of disinfectants to mitigate unintended consequences on gut health and maintain immune system integrity.