Inflammatory bowel disease (IBD) is a chronic condition that afflicts individuals repeatedly and cannot be cured at present, which has seriously affected the quality of life of patients. Minerals Containing Rubidium (MCR) from Guangxi Yuechengling, which Professor Zhao Lichun purified, were explored. Against this backdrop, the present study investigates the efficacy of rubidium salt in ulcerative colitis. Rubidium salt reduced levels of inflammatory markers and improved intestinal barrier function through the Elisa kit, immunohistochemistry, and qPCR. Next, we detected the level of short-chain fatty acid and found that the content of propanoic acid, butyric acid, and n-butyric acid increased after treatment with rubidium salt. We used fecal metagenomics to explore the underlying reasons further and found that rubidium salt significantly adjusted the structure of intestinal flora, increased the abundance of beneficial bacteria such as lactobacillus and bifidobacterium, and inhibited the abundance of harmful bacteria such as Enterobacteriaceae and Escherichia coli. We also learned that rubidium salt directly weakened pathogenic bacteria's infection and survival ability by reducing the expression of virulence factors such as fimH, invA, and hilA and virulence genes such as acrA and ompR. Overall, rubidium salt can reduce harmful bacteria and increase beneficial bacteria. The increased beneficial bacteria help enhance the gut barrier and regulate inflammatory factors by raising the levels of short-chain fatty acids. A strengthened gut barrier further stabilizes microbial homeostasis, ultimately alleviating ulcerative colitis.

Bacterial assemblages associated with sea urchin are critical to their physiology and ecology within marine ecosystems. In this study, we characterized the bacterial communities in wild sea urchin Anthocidaris crassispina captured in Daya Bay, South China Sea. A total of 363 amplicon sequence variants belonging to nine phyla and 141 genera were classified from intestine, body surface, and surrounding seawater samples. Proteobacteria, Firmicutes, and Bacteroidetes were the dominant bacteria phyla found in this study. A network analysis of bacterial interspecies interactions revealed varying complexity, stability, connectivity, and relationship patterns across the samples, with the most intricate network observed in the surrounding seawater. Metagenomic predictions highlighted the distinct bacterial metabolic pathways, with significant differences between intestine and seawater samples. Notably, pathways associated with polysaccharide degradation, including chitin derivatives, starch, and CoM biosynthesis, were markedly abundant, underscoring the gut microbiota's key role in digesting algae. In addition, other metabolic pathways in intestine samples were linked to immune response regulation of sea urchins. Overall, this study provides a comprehensive overview of the bacterial community structure and potential functional roles in A. crassispina.

In this study, 2 types of drinking water were provided to broiler chicks to evaluate the relationship between the bacterial load of drinking water and cecal microbiota. One type of drinking water was untreated, while the other type was daily treated with sodium dichlorocyanurate (50 mg/L). A total of 240 broiler chicks were divided into 2 groups based on their initial body weight. There were 6 replicates in each group, and each replicate cage contained 20 birds. Each cage was assigned to a different floor of the battery cage. On the final day, water samples were collected from each replicate cage at the opening of the drinking cup height, and one bird was selected from each replicate cage to obtain cecal content samples for measuring microbiota composition using the 16S rRNA technique. We found that drinking water treated with sodium dichlorocyanurate significantly reduced the richness and diversity of microbiota and diminished/disappeared most gram-negative bacteria. Broiler chicks that consumed chlorinated drinking water exhibited changes in the composition of cecal microbiota, with Alistipes serving as the marker species in the cecal content of broiler chicks that consumed untreated water, whereas AF12 served as the marker species in the cecal content of broiler chicks that consumed chlorinated drinking water. Functional prediction using the MetaCyc database and species composition analysis of metabolic pathways showed that changes in 7 metabolic pathways were related to the abundance of Providencia. Therefore, we concluded that chlorinated drinking water reduced the bacterial load in drinking water, thereby altering the cecal microbiota composition and regulating the metabolic activity of broiler chicks.

Inflammatory bowel diseases (IBD) involve complex interactions among genetic factors, aberrant immune activation, and gut microbial dysbiosis. While metabolomic studies have focused on feces and serum, fewer investigations have examined the intestinal mucosa despite its crucial role in metabolite absorption and transport. The goals of this study were twofold: to test the hypothesis that gut microbial dysbiosis from chronic intestinal inflammation leads to mucosal metabolic alterations suitable for therapeutic targeting, and to address gaps in metabolomic studies of intestinal inflammation that have overlooked the mucosal metabolome. The chronic DSS colitis was induced for five weeks in 7-9-week-old wild-type C57BL/6J male mice followed by microbial profiling with targeted 16srRNA sequencing service. Mucosal metabolite measurements were performed by Metabolon (Morrisville, NC). The data were analyzed using the bioinformatic tools Pathview, MetOrigin, and Metaboanalyst. The novel findings demonstrated increases in several host- and microbe-derived purine, pyrimidine, endocannabinoid, and ceramide metabolites in colitis. Origin analysis revealed that microbial-related tryptophan metabolites kynurenine, anthranilate, 5-hydroxyindoleacetate, and C-glycosyltryptophan were significantly increased in colon mucosa during chronic inflammation and strongly correlated with disease activity. These findings offer new insights into the pathophysiology of IBD and provide novel potential targets for microbial-based therapeutics.

This study aimed to understand the structural, digestion and fecal fermentation behaviors of sea cucumber polysaccharide fermented by Bacillus subtilis Natto. Results showed that both sea cucumber polysaccharide (SP) and fermented sea cucumber polysaccharide (FSP) were sulfated polysaccharides mainly containing fucose. The physicochemical property, molecular weight, thermal property, and functional groups were no significant difference between SP and FSP, but the microscopic morphology and monosaccharide composition of FSP changed. Both SP and FSP showed similar digestion and fecal fermentation characteristics, that is, they could not be digested by saliva and gastric juice, but could be partially degraded by small intestine. Due to the decomposition of glycosidic bonds after intestinal digestion and fecal fermentation, the relative molecular mass of SP and FSP decreased. In terms of impacts on gut microbiota, Lachnospira, Bacteroides finegoldii, and Bifidobacteriaceae were significantly increased in SP, while Acinetobacter was significantly increased in FSP. This study provides a good understanding of the changes in the structure and digestive characteristics of sea cucumber polysaccharides caused by fermentation. That information will be beneficial for the development and application of new fermented sea cucumber products.

Acinetobacter infections have high rates of mortality due to an increasing incidence of infections by multidrug-resistant (MDR) and extensively-drug-resistant (XDR) strains. Therefore, new therapeutic strategies for the treatment of Acinetobacter infections are urgently needed. Acinetobacter spp. are Gram-negative coccobacilli that are obligate aerobes and can utilize a wide variety of carbon sources. Acinetobacter baumannii is the main cause of Acinetobacter infections, and recent work has identified multiple strategies A. baumannii uses to acquire nutrients and replicate in the face of host nutrient restriction. Some host nutrient sources also serve antimicrobial and immunomodulatory functions. Hence, understanding Acinetobacter metabolism during infection may provide new insights into novel infection control measures. In this review, we focus on the role of metabolism during infection and in resistance to antibiotics and other antimicrobial agents and discuss the possibility that metabolism may be exploited to identify novel targets to treat Acinetobacter infections.

Bacterial pneumonia is a common infection of the lower respiratory tract that can afflict patients of all ages. Multidrug-resistant strains of Acinetobacter baumannii are increasingly responsible for causing nosocomial pneumonias, thus posing an urgent threat. Alveolar macrophages play a critical role in overcoming respiratory infections caused by this pathogen. Recently, we and others have shown that new clinical isolates of A. baumannii, but not the common lab strain ATCC 19606 (19606), can persist and replicate in macrophages within spacious vacuoles that we called Acinetobacter Containing Vacuoles (ACV). In this work, we demonstrate that the modern A. baumannii clinical isolate 398, but not the lab strain 19606, can infect alveolar macrophages and produce ACVs in vivo in a murine pneumonia model. Both strains initially interact with the alveolar macrophage endocytic pathway, as indicated by EEA1 and LAMP1 markers; however, the fate of these strains diverges at a later stage. While 19606 is eliminated in an autophagy pathway, 398 replicates in ACVs and are not degraded. We show that 398 reverts the natural acidification of the phagosome by secreting large amounts of ammonia, a by-product of amino acid catabolism. We propose that this ability to survive within macrophages may be critical for the persistence of clinical A. baumannii isolates in the lung during a respiratory infection.

Gut microbiota was only considered as a commensal organism that aids in digestion, but recent studies revealed that the microbiome play a critical role in both physiological and pathological immune system. The gut microbiome composition is altered by environmental factors such as diet and hygiene, and the alteration affects immune cells, especially T cells. Advanced genomic techniques in microbiome research defined that specific microbes regulate T cell responses and the pathogenesis of immune-mediated disorders. Here, we review features of specific microbes-T cell crosstalk and relationship between the microbes and immunopathogenesis of diseases including in cancers, autoimmune disorders and allergic inflammations. We also discuss the limitations of current experimental animal models, cutting-edge developments and current challenges to overcome in the field, and the possibility of considering gut microbiome in the development of new drug.

Ulcerative colitis (UC) is a chronic nonspecific inflammatory disease with a complex etiology. Intestinal mucosal injury is an important pathological change in individuals with UC. Leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5+) intestinal stem cells (ISCs) exhibit self-renewal and high differentiation potential and play important roles in the repair of intestinal mucosal injury. Moreover, LGR5+ ISCs are intricately regulated by both the Wnt/β-catenin and Notch signaling pathways, which jointly maintain the function of LGR5+ ISCs. Combination therapy targeting multiple signaling pathways and transplantation of LGR5+ ISCs may lead to the development of new clinical therapies for UC.

Background: Acinetobacter spp. have emerged as troublesome pathogens due to their multi-drug resistance. The majority of the work to date has focused on the antibiotic resistance profile of Acinetobacter baumannii. Although A. calcoaceticus strains are isolated in the hospital setting, limited information is available on these closely related species. Methods & Results: The computational analysis of antibiotic resistance genes in 1441 Acinetobacter genomes revealed that A. calcoaceticus harbored a similar repertoire of multi-drug efflux pump and beta-lactam resistance genes as A. baumannii, leading us to speculate that A. calcoaceticus would have a similar antibiotic resistance profile to A. baumannii. To profile the resistance patterns of A. calcoaceticus, strains were examined by Kirby−Bauer disk diffusion and phenotypic microarrays. We found that Acinetobacter strains were moderately to highly resistant to certain antibiotics within fluoroquinolones, aminoglycosides, tetracyclines, and other antibiotic classes. These data indicate that A. calcoaceticus has a similar antibiotic resistance profile as A. baumannii ATCC 19606. We also identified that all Acinetobacter species were sensitive to 5-fluoroorotic acid, novobiocin, and benzethonium chloride. Conclusion: Collectively, these data provide new insights into the antibiotic resistance in A. calcoaceticus and identify several antibiotics that could be beneficial in treating Acinetobacter infections.