The synergistic effect of Levilactobacillus brevis IBRC-M10790 and vitamin D3 on Helicobacter pylori-induced inflammation.

Background: Owing to the emergence and spread of multidrug resistance mechanisms in Helicobacter pylori, achieving a successful eradication has become exceedingly difficult. Thus, this study for the first time determines the effect of a combination of vitamin D3 and probiotic on the pathogenesis and treatment of H. pylori. Methods: We established an in vitro experimental system using AGS human gastric carcinoma cells and explored the synergistic effect of Levilactobacillus brevis IBRC-M10790 and vitamin D3 on H. pylori. Live and pasteurized L. brevis, L. brevis-derived membrane vesicles (MVs), and L. brevis cell-free supernatant (CFS), as well as their combination with vitamin D3 were used during this study. We assessed the anti-inflammatory and anti-oxidative effects of these combinations using RT-qPCR and ELISA, respectively. We further performed an adhesion assay to evaluate the influence of L. brevis and vitamin D3 on the adherence rate of H. pylori to AGS cells. Results: Our results demonstrated that L. brevis and vitamin D3 possess anti-inflammatory and anti-oxidative effects against H. pylori infection in AGS cells. The combination of vitamin D3 with the probiotic strain (particularly live L. brevis and its CFS) can more efficiently reduce the expression of pro-inflammatory cytokines IL-6, IL-8, IFN-γ, and TNF-α in the AGS cells. Moreover, vitamin D3 and L. brevis exhibited an additive impact preserving the integrity of the epithelial barrier by increasing the expression of the tight junction protein ZO-1. Furthermore, this combination can potentially reduce H. pylori adherence to AGS cells. Conclusions: This study indicates the advantage of combining vitamin D3 and probiotic to attenuate H. pylori-induced inflammation and oxidative stress. Consequently, probiotic and vitamin D3 co-supplementation can be considered as a novel therapeutic approach to manage and prevent H. pylori infection.

The double-edged sword of probiotic supplementation on gut microbiota structure in Helicobacter pylori management.

As Helicobacter pylori management has become more challenging and less efficient over the last decade, the interest in innovative interventions is growing by the day. Probiotic co-supplementation to antibiotic therapies is reported in several studies, presenting a moderate reduction in drug-related side effects and a promotion in positive treatment outcomes. However, the significance of gut microbiota involvement in the competence of probiotic co-supplementation is emphasized by a few researchers, indicating the alteration in the host gastrointestinal microbiota following probiotic and drug uptake. Due to the lack of long-term follow-up studies to determine the efficiency of probiotic intervention in H. pylori eradication, and the delicate interaction of the gut microbiota with the host wellness, this review aims to discuss the gut microbiota alteration by probiotic co-supplementation in H. pylori management to predict the comprehensive effectiveness of probiotic oral administration.Abbreviations: acyl-CoA- acyl-coenzyme A; AMP- antimicrobial peptide; AMPK- AMP-activated protein kinase; AP-1- activator protein 1; BA- bile acid; BAR- bile acid receptor; BCAA- branched-chain amino acid; C2- acetate; C3- propionate; C4- butyrate; C5- valeric acid; CagA- Cytotoxin-associated gene A; cAMP- cyclic adenosine monophosphate; CD- Crohn's disease; CDI- C. difficile infection; COX-2- cyclooxygenase-2; DC- dendritic cell; EMT- epithelial-mesenchymal transition; FMO- flavin monooxygenases; FXR- farnesoid X receptor; GPBAR1- G-protein-coupled bile acid receptor 1; GPR4- G protein-coupled receptor 4; H2O2- hydrogen peroxide; HCC- hepatocellular carcinoma; HSC- hepatic stellate cell; IBD- inflammatory bowel disease; IBS- irritable bowel syndrome; IFN-γ- interferon-gamma; IgA immunoglobulin A; IL- interleukin; iNOS- induced nitric oxide synthase; JAK1- janus kinase 1; JAM-A- junctional adhesion molecule A; LAB- lactic acid bacteria; LPS- lipopolysaccharide; MALT- mucosa-associated lymphoid tissue; MAMP- microbe-associated molecular pattern; MCP-1- monocyte chemoattractant protein-1; MDR- multiple drug resistance; mTOR- mammalian target of rapamycin; MUC- mucin; NAFLD- nonalcoholic fatty liver disease; NF-κB- nuclear factor kappa B; NK- natural killer; NLRP3- NLR family pyrin domain containing 3; NOC- N-nitroso compounds; NOD- nucleotide-binding oligomerization domain; PICRUSt- phylogenetic investigation of communities by reconstruction of unobserved states; PRR- pattern recognition receptor; RA- retinoic acid; RNS- reactive nitrogen species; ROS- reactive oxygen species; rRNA- ribosomal RNA; SCFA- short-chain fatty acids; SDR- single drug resistance; SIgA- secretory immunoglobulin A; STAT3- signal transducer and activator of transcription 3; T1D- type 1 diabetes; T2D- type 2 diabetes; Th17- T helper 17; TLR- toll-like receptor; TMAO- trimethylamine N-oxide; TML- trimethyllysine; TNF-α- tumor necrosis factor-alpha; Tr1- type 1 regulatory T cell; Treg- regulatory T cell; UC- ulcerative colitis; VacA- Vacuolating toxin A.

The Effects of Vitamins and Micronutrients on Helicobacter pylori Pathogenicity, Survival, and Eradication: A Crosstalk between Micronutrients and Immune System.

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.

Management of multi-drug resistant Helicobacter pylori infection by supplementary, complementary and alternative medicine; a review.

Helicobacter pylori is recognized as the most common bacterial pathogens colonizing the gastric epithelium of nearly half of the world's population. This bacterium is the main etiological cause of gastroduodenal ulcers, and more importantly as the substantial risk factor for development of gastric cancer. The emergence and rapid increase in the prevalence of multi-drug resistant phenotypes have posed major pitfalls in effectiveness of various treatment regimens and eradication strategies against H. pylori infections. Several natural products and supplementary food components have been reported to have established anti-H. pylori activity. Herein, we review the application and efficacy of some specific natural products and foodstuffs such as milk, bee products (honey and propolis), fish oil, vitamins C and E, and also a nickel free-diet used as anti-H. pylori alternative treatment regimens.