Probiotic BIFICO cocktail ameliorates Helicobacter pylori induced gastritis

AIM: To determine the protective effect of triple viable probiotics on gastritis induced by Helicobacter pylori (H. pylori) and elucidate the possible mechanisms of protection. METHODS: Colonization of BIFICO strains in the mouse stomach was determined by counting colony-forming units per gram of stomach tissue. After treatment with or without BIFICO, inflammation and H. pylori colonization in the mouse stomach were analyzed by hematoxylin and eosin and Giemsa staining, respectively. Cytokine levels were determined by enzyme-linked immunosorbent assay and Milliplex. The activation of nuclear factor (NF)-kappa B and MAPK signaling in human gastric epithelial cells was evaluated by Western blot analysis. Quantitative reverse transcription-polymerase chain reaction was used to quantify TLR2, TLR4 and MyD88 mRNA expression in the mouse stomach. RESULTS: We demonstrated that BIFICO, which contains a mixture of Enterococcus faecalis, Bifido-bacterium longum and Lactobacillus acidophilus, was tolerant to the mouse stomach environment and was able to survive both the 8-h and 3-d courses of administration. Although BIFICO treatment had no effect on the colonization of H. pylori in the mouse stomach, it ameliorated H. pylori -induced gastritis by significantly inhibiting the expression of cytokines and chemokines such as TNF-alpha, IL-1 beta, IL-10, IL-6, G-CSF and MIP-2 (P < 0.05). These results led us to hypothesize that BIFICO treatment would diminish the H. pylori-induced inflammatory response in gastric mucosal epithelial cells in vitro via the NF-kappa B and MAPK signaling pathways. Indeed, we observed a decrease in the expression of the NF-kappa B subunit p65 and in the phosphorylation of I kappa B-alpha, ERK and p38. Moreover, there was a significant decrease in the production of IL-8, TNF-alpha, G-CSF and GM-CSF (P < 0.05), and the increased expression of TLR2, TLR4 and MyD88 induced by H. pylori in the stomach was also significantly reduced following BIFICO treatment (P < 0.05). CONCLUSION: Our results suggest that the probiotic cocktail BIFICO can ameliorate H. pylori-induced gastritis by inhibiting the inflammatory response in gastric epithelial cells.

Author Correction:Priming with FLO8-deficient Candida albicans induces Th1-biased protective immunity against lethal polymicrobial sepsis

In this article,which was published online on 5 Nov 2020,an unintended error occurred during the image processing of Fig.7J.In detail,the image for the control group in Figure 7J(left panel)was inadvertently captured from the same field in the IFN-γneutralizing group(Figure 7J,right panel).We have re-selected the pathological images of the control group in Figure 7J(left panel)from the raw data and corrected Figure 7J accordingly.The corrected Figure 7 is presented below.The error and correction did not impact the conclusion of the paper.The authors sincerely regret this error.The original article has been corrected.

Priming with FLO8-deficient Candida albicans induces Th1-biased protective immunity against lethal polymicrobial sepsis

The morphological switch between yeast and hyphae of Candida albicans is essential for its interaction with the host defense system.However,the lack of understanding of host-pathogen interactions during C.albicans infection greatly hampers the development of effective immunotherapies.Here,we found that priming with the C.albicans FLO8-deficient(flo8)mutant,locked in yeast form,protected mice from subsequent lethal C.albicans infection.Deficiency of Dectin-2,a fungus-derivedα-mannan recognition receptor,completely blocked flo8 mutant-induced protection.Mechanistically,the flo8 mutant-induced Dectin-2/CARD9-mediated IL-10 production in DCs and macrophages to block thymus atrophy by inhibiting the C.albicans-induced apoptosis of thymic T cells,which facilitated the continuous output of naive T cells from the thymus to the spleen.Continuous recruitment of naive T cells to the spleen enhanced Th1-biased antifungal immune responses.Consequently,depletion of CD4^(+)T cells or blockade of IL-10 receptor function using specific antibodies in mice completely blocked the protective effects of flo8 mutant priming against C.albicans infection.Moreover,mannans exposed on the surface of the flo8 mutant were responsible for eliciting protective immunity by inhibiting the C.albicans-induced apoptosis of thymic T cells to sustain the number of naive T cells in the spleen.Importantly,priming with the flo8 mutant extensively protected mice from polymicrobial infection caused by cecal ligation and puncture(CLP)by enhancing Th1-biased immune responses.Together,our findings imply that targeting FLO8 in C.albicans elicits protective immune responses against polymicrobial infections and that mannans extracted from the flo8 mutant are potential immunotherapeutic candidate(s)for controlling infectious diseases.