Hepcidin is the primary regulator of vertebrate iron homeostasis. Its production is stimulated by systemic iron levels and inflammatory signals. Although the role of hepcidin in iron homeostasis is well characterized, its response to pathogenic agents is complex and diverse. In this review, we examine studies that investigate the role of hepcidin in response to infectious agents. Interleukin-6 (IL-6) is a key factor responsible for the induction of hepcidin expression. During infection, hepcidin-mediated depletion of extracellular iron serves as a protective mechanism against a variety of pathogens. However, accumulation of iron in macrophages through hepcidin-mediated pathways may increase susceptibility to intracellular pathogens such as Mycobacterium tuberculosis. Prolonged elevation of hepcidin production can lead to anemia due to reduced iron availability for erythropoiesis, a condition referred to as anemia of inflammation. In addition, we highlight the role of hepcidin upregulation in several infectious contexts, including HIV-associated anemia, iron deficiency anemia in Helicobacter pylori infection, and post-malarial anemia in pediatric patients. In addition, we show that certain infectious agents, such as hepatitis C virus (HCV), can suppress hepcidin production during both the acute and chronic phases of infection, while hepatitis B virus (HBV) exhibits similar suppression during the chronic phase.

Oxidative stress contributes to the development of cardiometabolic diseases and cancers. Numerous studies have highlighted the adverse effects of high reactive oxygen species (ROS) levels in the progression of chronic noncommunicable diseases and also during infections. On the other hand, antioxidants play a crucial role in preventing oxidative stress or postponing cell damage via the direct scavenging of free radicals or indirectly via the Keap1/Nrf2/ARE pathway, among others. Dietary antioxidants can be obtained from various sources, mainly through a plant-based diet, including fruits and vegetables. The dietary antioxidant index (DAI) has been developed to assess total antioxidant intake from diet. This review delineated the performance of DAI in the risk assessment of different diseases. It is suggested that a high DAI score prevents obesity-related diseases, including diabetes mellitus, hyperuricemia, dyslipidemia, and metabolic (dysfunction)-associated steatotic liver disease (MASLD). Additionally, DAI is negatively associated with Helicobacter pylori and Human papillomavirus infection, thus reducing the risk of gastric and cervical cancer. Also, a high intake of antioxidants prevents the development of osteoporosis, miscarriage, infertility, and mental illnesses. However, further prospective observations and clinical trials are warranted to confirm the application of DAI in preventing diseases that have been studied.

Helicobacter pylori is a type of Gram-negative microaerobic bacteria that inhabits the gastric mucosal epithelium. It can cause various gastrointestinal diseases including gastritis, peptic ulcer and gastric cancer. White blood cells (WBC) are common immune cells, the increase in whose countoften indicates the presence of an infection. Currently, the relationship between H. pylori and WBC count remains full of controversy. This study aims to further elucidate the effects of H. pylori on WBC count in a population undergoing physical examination.

A total of 864 participants who underwent physical examination and 14C urea breath test (UBT) were retrospectively enrolled in this study from January to June 2021. The overall population was divided into H. pylori-negative (Hp-) and H. pylori-positive (Hp+) groups based on the disintegration per minute (DPM) value detected by UBT. Spearman's correlation analysis was used to assess the correlation between DPM and WBC count. General linear regression models were applied to assess the potential factors contributing to the increase in WBC count. Generalised additive model (GAM) was performed to identify the non-linear relationship between DPM and WBC count. Additionally, a piecewise linear regression was used to examine the threshold effect of the DPM on WBC count.

403 subjects were diagnosed with H. pylori infection. The WBC and platelet (PLT) counts in the Hp+ group were significantly higher than those in the Hp- group. Additionally, the prevalence of H. pylori infection gradually increased with the WBC count quartiles (38.89% and 54.67% in quartile 1 and quartile 4, respectively). Spearman's correlation analysis showed that the DPM value significantly correlated with WBC count (r=0.089, p=0.009) and PLT count (r=0.082, p=0.017). The linear model revealed a positive independent association of H. pylori infection and DPM with WBC count (βHp+=0.398 (95% CI 0.170, 0.625), p<0.001; βDPM=0.002 (95% CI 0.000, 0.0030), p=0.018). The results of the GAM and the piecewise linear regression suggested that the cut-off points of the association between DPM and WBC count were 40 and 155 of DPM, that is, the effect of DPM on WBC count varied with the difference of DPM <40, 40-155, and >155 (βDPM=-0.005 (95% CI -0.017, 0.007), p=0.423; βDPM=0.006 (95% CI 0.002, 0.013), p=0.047; and βDPM=-0.007 (95% CI -0.012, -0.002), p=0.004, respectively).

H. pylori infection was independently and positively correlated with WBC count; however, the effect of DPM on WBC count varied across different WBC count intervals, suggesting distinct immunological responses at different stages of infection.

The prevalence of Helicobacter pylori (H. pylori) infection and its potential relationship to various diseases is currently a focus of attention. The aim of this study is to investigate the association between current and past H. pylori infections and elevated levels of microalbuminuria in type 2 diabetic patients.

Two hundred patients with type 2 diabetes mellitus were tested for the presence of H. pylori infection. They were divided into three groups: 52 had a current H. pylori infection, 38 had a past H. pylori infection, and 110 had no H. pylori infection. All study participants underwent assessments of plasma glucose levels, glycated hemoglobin (HbA1c), albuminuria levels, inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), as well as other relevant investigations.

The prevalence of H. pylori infection (current and past) was detected in 90 out of 200 diabetic patients (45%). There was no statistically significant difference between the three groups in terms of age, diabetes duration, family history of DM, family history of hypertension, residence, or dyspeptic symptoms, indicating that current or past infection with H. pylori has no association with these variables. The current H. pylori infection group showed the highest levels of inflammatory markers, ESR and CRP, which were significantly different from those in the non-infected group (p = 0.013 and p < 0.001, respectively). The median (IQR) of albuminuria levels in the current H. pylori infection group, the past H. pylori infection group, and the non-infected group were 125 (4.8-290), 7.6 (2.4-271), and 5.1 (1.2-173), respectively. The current H. pylori infection group showed the highest albuminuria level, which was significantly different from that of the non-infected group (p = 0.001).

There might be an association between microalbuminuria levels, general inflammatory markers (ESR and CRP), and current H. pylori infection in type 2 diabetic patients.

Background and objective Iron deficiency and iron deficiency anemia are related but distinct conditions. Iron deficiency refers to a state where the body has insufficient iron stores, which can lead to anemia if not addressed. Iron deficiency anemia, on the other hand, is a more severe condition where the lack of iron has resulted in decreased hemoglobin levels, impacting oxygen transport in the blood. Helicobacter pylori (H. pylori) infection can contribute to iron deficiency through mechanisms such as chronic gastrointestinal bleeding and impaired iron absorption, potentially progressing to iron deficiency anemia. The objective of this study was to determine the prevalence of iron deficiency, including its potential progression to iron deficiency anemia, among patients diagnosed with H. pylori infection. Methodology This cross-sectional study was conducted at Bolan Medical Complex Hospital, Quetta, and included 200 patients diagnosed with H. pylori infection via endoscopic biopsy or urea breath test, from January to June 2023. Participants were aged 18 years and older, excluding those with chronic diseases affecting iron metabolism, current iron supplement users, and pregnant women. Data were collected through questionnaires and medical records, and blood samples were analyzed for serum ferritin and hemoglobin levels. Statistical analysis included chi-square tests and logistic regression was performed in SPSS (version 27; IBM Corp, Armonk, NY); p-value <0.05 was significant. Results Out of 200 patients, 80 (40%) were iron deficient. The prevalence was highest among those over 60 years (n = 15, 75%) compared to the 18-30 age group (n = 10, 20%). Males had a slightly higher prevalence of iron deficiency (n = 50, 45.5%) compared to females (n = 30, 33.3%). Patients with H. pylori infection for more than three years exhibited a higher prevalence of iron deficiency (n = 30, 50%) compared to those with less than one year of infection (10/60, 16.7%). Dietary habits also played a role, with vegetarians showing a higher prevalence (n = 20, 50%) compared to non-vegetarians (n = 60, 37.5%). Hemoglobin levels were significantly lower in iron-deficient participants, averaging 10.8 ± 0.9 g/dL, and logistic regression indicated significant associations between iron deficiency and both age (OR = 1.05, p = 0.001) and infection duration (OR = 1.10, p < 0.001). Conclusions The study revealed a significant prevalence of iron deficiency among H. pylori-infected patients, particularly in older adults, males, those with longer infection duration, and vegetarians. The findings underscore the need for routine monitoring and targeted treatment of iron deficiency in this population.

Dyspepsia is a common gastrointestinal illness sometimes associated with Helicobacter pylori (H. pylori) infection. Screening and eradicating the bacterium reduces the risk of infection-related complications. The aim of this study was to determine the magnitude of H. pylori infection among dyspeptic patients and the effectiveness of triple eradication therapy at hospitals in Hawassa city, Ethiopia.

The prevalence of H. pylori infection was 48.5%. The H. pylori eradication rate using first-line triple therapy was 83.8%. Eradication therapy failure is associated with previous exposure compared to no exposure (AOR: 4.8, 95% CI: 1.37-10.97), a regimen for 10-days compared to 14-days (AOR: 4.05, 95% CI: 1.42-11.55), and self-reported side effects compared to no report (AOR: 2.5, 95% CI: 1.12-5.97). Based on Morisky-eight scale 230 (79.0%) patients were adherent to their triple therapy. Participants with no reports of adverse effects showed increased odds of adherence to triple therapy compared to those who had reports (AOR = 2.45, 95% CI: 1.29-4.62).

This study demonstrated that about half of adult dyspeptic patients were infected with H. pylori, and moderate eradication was observed. Factors such as previous history of eradication therapy, duration of the eradication regimen, and perception of potential adverse effects are associated with eradication rate and should be considered during the initiation of eradication therapy.

H. pylori (ubiquitous) and anemia together represent one of the growing health concerns globally. Gastroduodenal sequelae of H. pylori infection are distinguished; however, for the H. pylori infection and its implication in the development of anemia, iron has a significant health impact. We aimed to evaluate H. pylori infection-associated anemia by employing a logistic regression analysis model. A retrospective (case-control) study design-based assessment of the H. pylori associated-anemia. The study area was geo-referenced by QGIS/QuickMapServies. Descriptive and inferential statistical analyses were accomplished using the R-base-R-studio (v-4.0.2)-tidyverse. A p-value < 0.05 was the statistical significance cut-off value. A ggplot2 package was used for data representation and visualization. Mean ± SD age, Hb, MCV, ferritin, and RBC for overall study participants were measured to be 44.0 ± 13.58, 13.84 ± 2.49, 83.02 ± 8.31, 59.42 ± 68.37, and 5.14 ± 0.75, respectively. Decreased levels of Hb (infected vs. uninfected: 13.26 ± 2.92 vs. 14.42 ± 1.75, p < 0.001) ferritin (infected vs. uninfected: 48.11 ± 63.75 vs. 71.17 ± 71.14, p < 0.001), and MCV (infected vs. uninfected: 81.29 ± 9.13 vs. and 84.82 ± 6.93, p < 0.05) were measured to be associated with H. pylori infection when compared with H. pylori uninfected control group. Moreover, the magnitude (prevalence) of anemia (infected vs. uninfected: 78% vs. 21%, p < 0.001), iron deficiency anemia (IDA) (infected vs. uninfected: 63.3% vs. 36.6%, p < 0.001), and microcytic anemia (infected vs. uninfected: 71.6% vs. 46.1%, p < 0.001) were significantly different among the H. pylori-infected participants. The higher likelihood of developing anemia (AOR; 4.98, 95% CI; 3.089-8.308, p < 0.001), IDA (AOR; 3.061, 95% CI; 2.135-4.416, p < 0.001), and microcytic anemia (AOR; 3.289, 95% CI; 2.213-4.949, p < 0.001) by 398%, 206.1%, and 229%, respectively, was associated with H. pylori-infected. We recommend the regular monitoring of hematological parameters and eradication of H. pylori infection to minimize the extra-gastric health consequences of H. pylori infection.

To determine the prevalence of anemia and its association with Helicobacter pylori infection among adult dyspeptic patients.

A cross-sectional study was conducted among 283 dyspeptic patients at Kiryandongo General Hospital, in Uganda. A structured questionnaire was administered to capture demographic and clinical characteristics of study participants. Four milliliters of blood were then collected into an EDTA vacutainer for Complete Blood Count (CBC) and analyzed using HUMA COUNT 30^TS, and peripheral blood smears were made and stained using Giemsa stain. Anemia was defined as hemoglobin levels <12g/dl in females and <13g/dl in men according to the World Health Organization (WHO). Helicobacter pylori (H. pylori) stool antigen test was performed using Whole power H. pylori Ag rapid test device, and saline stool preparation was examined for intestinal parasites. Chi-squared test and Logistic regression were performed to determine association, and a p-value of ≤0.05 was considered statistically significant.

The overall prevalence of Helicobacter pylori infection was 42.4% (120/283). The prevalence of anemia among H. pylori-infected patients was 25.8% (31/120) and 15.3% (25/163) among H. pylori-negative counterparts. H. pylori infection was significantly associated with anemia (p-value 0.042), age (p-value 0.02, 0.009), water sources (p-value 0.0049,) and intestinal parasitic infestation (p-value 0.02), respectively.

This study has shown that the prevalence of H. pylori infection and anemia is high among dyspeptic patients at Kiryandongo General Hospital. H. pylori infection was found associated with anemia, age, water sources, and intestinal parasitic infestation. Routine screening of anemia in H. pylori-infected individuals and further studies to explore the relationship between anemia and H. pylori disease is highly recommended.

Helicobacter pylori (HP) is a Gram-negative bacterium that colonizes the human stomach chronically. Colonization of HP in the gastric mucosa not only causes gastrointestinal diseases, but also is associated with extra-gastric diseases, such as idiopathic thrombocytopenic purpura and neurological diseases. Among neurological diseases, epidemiological studies have shown that HP infection increases the prevalence of Alzheimer's disease (AD) and Parkinson's disease (PD). Since HP does not invade the central nervous system (CNS), it has been considered that systemic immunological changes induced by HP infection may play pathogenic roles in AD and PD. Here, we investigated the effects of HP infection on the CNS in vivo and in vitro. In the CNS, chronically HP-infected mice had microglial activation without HP colonization, although systemic immunological changes were not observed. This led us to explore the possibility that HP-derived outer membrane vesicles (HP-OMVs) could cause neuroinflammation. OMVs are small, spherical bilayer vesicles (20-500 nm) released into the extracellular space from the outer membrane of Gram-negative bacteria; OMVs contain lipopolysaccharide, proteins, peptidoglycan, DNA, and RNA. OMVs have also been shown to activate both innate and acquired immune cells in vitro, and to disrupt the tight junctions of the gastric epithelium ("leaky gut") as well as cross the blood-brain barrier in vivo. Thus, in theory, OMVs can activate immune responses in the remote organs, including the lymphoid organs and CNS, if only OMVs enter the systemic circulation. From the exosome fraction of sera from HP-infected mice, we detected HP-specific DNA, suggesting the presence of HP-OMVs. We also found that microglia incubated with HP-OMVs in vitro increased the cell proliferation, inflammatory cytokine production, and migration. On the other hand, HP-OMVs suppressed the cell proliferation of neuroblastoma in vitro. Lastly, we found that AD model mice infected with HP had amyloid plaques adjacent to activated microglia and astrocytes in vivo. Based on the literature review and our experimental data, we propose our working hypothesis that OMVs produced in chronic HP infection in the gut induce neuroinflammation in the CNS, explaining the higher prevalence of AD in HP-infected people.

Helicobacter pylori as a class I carcinogen is correlated with a variety of severe gastroduodenal diseases; therefore, H. pylori eradication has become a priority to prevent gastric carcinogenesis. However, due to the emergence and spread of multidrug and single drug resistance mechanisms in H. pylori, as well as serious side effects of currently used antibiotic interventions, achieving successful H. pylori eradication has become exceedingly difficult. Recent studies expressed the intention of seeking novel strategies to improve H. pylori management and reduce the risk of H. pylori-associated intestinal and extragastrointestinal disorders. For which, vitamin supplementation has been demonstrated in many studies to have a tight interaction with H. pylori infection, either directly through the regulation of the host inflammatory pathways or indirectly by promoting the host immune response. On the other hand, H. pylori infection is reported to result in micronutrient malabsorption or deficiency. Furthermore, serum levels of particular micronutrients, especially vitamin D, are inversely correlated to the risk of H. pylori infection and eradication failure. Accordingly, vitamin supplementation might increase the efficiency of H. pylori eradication and reduce the risk of drug-related adverse effects. Therefore, this review aims at highlighting the regulatory role of micronutrients in H. pylori-induced host immune response and their potential capacity, as intrinsic antioxidants, for reducing oxidative stress and inflammation. We also discuss the uncovered mechanisms underlying the molecular and serological interactions between micronutrients and H. pylori infection to present a perspective for innovative in vitro investigations, as well as novel clinical implications.

Helicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the stomach and can induce gastric disease and intra-gastric lesions, including chronic gastritis, peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. This bacterium is responsible for long-term complications of gastric disease. The conjunction of host genetics, immune response, bacterial virulence expression, diet, micronutrient availability, and microbiome structure influence the disease outcomes related to chronic H. pylori infection. In this regard, the consumption of unhealthy and unbalanced diets can induce microbial dysbiosis, which infection with H. pylori may contribute to. However, to date, clinical trials have reported controversial results and current knowledge in this field is inconclusive. Here, we review preclinical studies concerning the changes produced in the microbiota that may be related to H. pylori infection, as well as the involvement of diet. We summarize and discuss the last approaches based on the modulation of the microbiota to improve the negative impact of H. pylori infection and their potential translation from bench to bedside.