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Proton pump inhibitors (PPIs) alter the composition of the intestinal microbiome, exacerbating indomethacin (IND)-induced small intestinal damage. Vonoprazan fumarate inhibits gastric acid secretion using a different mechanism from PPIs. We investigated the effects of both drugs on the intestinal microbiome and IND-induced small intestinal damage. We sought to clarify whether PPI-induced dysbiosis and worsening of the damage were due to a specific drug class effect of PPIs. Rabeprazole administration increased operational taxonomic unit numbers in the small intestines of C57BL/6 J mice, whereas the difference was not significant in the vonoprazan-treated group but exhibited a trend. Permutational multivariate analysis of variance of the unweighted UniFrac distances showed significant differences between vehicle- and vonoprazan- or rabeprazole-treated groups. L. johnsonii was the predominant microbial species, and the population ratio decreased after vonoprazan and rabeprazole administration. The vonoprazan- and rabeprazole-treated groups showed increased IND-induced damage. This high sensitivity to IND-induced damage was evaluated by transplantation with contents from the small intestine of mice treated with either vonoprazan or rabeprazole. Supplementation of L. johnsonii orally in mice treated with rabeprazole and vonoprazan prevented the increase in IND-induced small intestinal damage. In conclusion, both rabeprazole and vonoprazan aggravated NSAID-induced small intestinal injury by reducing the population of L. johnsonii in the small intestine via suppressing gastric acid secretion.

Lactobacillus johnsonii is a commensal bacterium isolated from the vaginal and gastrointestinal tracts of vertebrate hosts, including humans. It is a potential anti-inflammatory bacterium. As reported in many animal studies, L. johnsonii supplementation reduces inflammation in the intestine and enhances the epithelial barrier. However, in this study, we observed immunostimulatory effects of heat-killed L. johnsonii JERA01 (LJ) supplementation on antigen-presenting cells, such as dendritic cells and macrophages, in mice. LJ pretreatment increased the expression of maturation markers and TNF-α, IL-6, IL-12p40 production in bone marrow-derived dendritic cells and macrophages (BMDCs and BMDMs). Co-culture of LJ-pretreated BMDCs or BMDMs with lymphocytes enhanced IFN-γ production in vitro . Oral LJ (10 8 CFU) supplementation induced macrophage infiltration into the peritoneal cavity and Peyer’s patch at 12-h after administration, resulting in an increase in the population of IFN-γ-producing T cells in the Peyer’s patch. Our investigation revealed the effects of LJ, which activates macrophages and increases the Th-1 T cell population in the intestine, implying the possibility of using L. johnsonii as an immune stimulator.

In this study, we tested our hypothesis regarding mechanistic cross-talk between gastrointestinal inflammation and memory loss in a mouse model. Intrarectal injection of the colitis inducer 2,4,6-trinitrobenzenesulfonic acid (TNBS) in mice caused colitis via activation of nuclear factor (NF)-κB and increase in membrane permeability. TNBS treatment increased fecal and blood levels of lipopolysaccharide (LPS) and the number of Enterobacteriaceae, particularly Escherichia coli (EC), in the gut microbiota composition, but significantly reduced the number of Lactobacillus johnsonii (LJ). Indeed, we observed that the mice treated with TNBS displayed impaired memory, as assessed using the Y-maze and passive avoidance tasks. Furthermore, treatment with EC, which was isolated from the feces of mice with TNBS-induced colitis, caused memory impairment and colitis, and increased the absorption of orally administered LPS into the blood. Treatment with TNBS or EC induced NF-κB activation and tumor necrosis factor-α expression in the hippocampus of mice, as well as suppressed brain-derived neurotrophic factor expression. However, treatment with LJ restored the disturbed gut microbiota composition, lowered gut microbiota, and blood LPS levels, and attenuated both TNBS- and EC-induced memory impairment and colitis. These results suggest that the gut microbiota disturbance by extrinsic stresses can cause gastrointestinal inflammation, resulting in memory impairment.

Based on the microbiota–gut–brain axis (MGBA) hypothesis, probiotics play an increasingly important role in treating various psychiatric disorders. Schizophrenia (SCZ) is a common mental disease with a complex pathogenesis and is challenging to treat. Although studies have elucidated the mechanisms associated with the interactions between the microbiota–gut–brain axis and SCZ, few have specifically used probiotics as a therapeutic intervention for SCZ. Accordingly, the current study determines whether L. johnsonii YH1136 effectively prevents SCZ-like behavior in mice and identifies the associated key microbes and metabolites. An SCZ mouse model was established by intraperitoneal injection of MK-801; L. johnsonii YH1136 was administered via oral gavage. L. johnsonii YH1136 significantly improves abnormal behaviors, including psychomotor hyperactivity and sociability and alleviates aberrant enzyme expression associated with tryptophan metabolism in SCZ mice. Additionally, L. johnsonii YH1136 upregulates hippocampal brain-derived neurotrophic factor (BDNF) levels while downregulating tryptophan 2,3-dioxygenase (TDO2), indoleamine-pyrrole 2,3-dioxygenase 1 (IDO1), kynurenine aminotransferase 1 (KAT1). Subsequent 16S rRNA sequencing of intestinal contents suggests that L. johnsonii YH1136 modulates the gut flora structure and composition by increasing the relative abundance of Lactobacillus and decreasing Dubosiella in SCZ mice. N-acetylneuraminic acid and hypoxanthine are the key serum metabolites mediating the interaction between the MGBA and SCZ. These results partially reveal the mechanism underlying the effects of L. johnsonii YH1136 on SCZ-like behavior in mice, supporting the development of therapeutic L. johnsonii probiotic formulations against SCZ.

Lactobacillus johnsonii is a well-known probiotic species with health-beneficial properties, including host immunomodulation and pathogen inhibition. Its growing relevance in the medical industry highlights the need to understand its biology, particularly how it adapts to different host environments. In bacteria, niche adaptation is often accompanied by the loss or gain of coding sequences along with changes in the genome size. In this study, we explored the genetic diversity of L. johnsonii strains from the gastrointestinal tracts of various vertebrates such as rodents, birds, swine, and humans. We found associations between genome content and host species of origin and could conceptually demonstrate that these genes are being differentially transcribed under varying conditions. Several functions were associated with specific host groups, suggesting that L. johnsonii strains have adapted to their hosts over time.

Inflammatory bowel disease (IBD) remains a global health challenge linked to intestinal barrier disruption, microbiota dysbiosis, and immune dysregulation, though the interplay of these mechanisms remains poorly defined. Here, we investigated the therapeutic potential of Lactobacillus johnsonii N5 in a murine dextran sulfate sodium (DSS)-induced colitis model. Prophylactic N5 administration alleviated colitis symptoms (weight loss, colon shortening), reduced fecal and serum lipocalin-2 levels, and suppressed colonic pro-inflammatory cytokines (IL-1β, IL-6). N5 preserved microbial diversity, enhanced mucus secretion, and reinforced mucosal barrier integrity, preventing colitis onset. Therapeutically, N5 attenuated disease progression by downregulating IL-1β, IL-6, IL-8 expression, restoring Lactobacillus populations, and suppressing Escherichia-Shigella expansion, thereby reducing bacterial translocation and systemic inflammation. N5 promoted Ki67 + epithelial proliferation, accelerating mucosal repair. Mechanistically, N5 targeted neutrophil-mediated gut-liver injury, suppressing coagulation pathways in colon-liver transcriptomes, reducing hepatic lesions, platelet aggregation, CD162 + neutrophil recruitment, and H3cit + neutrophil extracellular trap (NET) formation. N5’s effects were partially recapitulated by DNase I in vivo and/or by its metabolites in vitro, suggesting its action involves metabolite-driven NET inhibition alongside DNase-like NET clearance. These findings illuminate N5’s dual role in IBD-prophylactic barrier fortification and therapeutic resolution of neutrophilic inflammation, and highlight its potential as a multifaceted probiotic therapy. Lactobacillus johnsonii N5 prevents colitis by fortifying the mucosal barrier and alleviates disease by inhibiting NETosis and gut-liver inflammation, promoting mucosal repair.

Abstract Some strains of lactic acid bacteria are reported to inhibit the growth of Helicobacter pylori and proposed to be useful to support so-called triple therapy for H. pylori. Although most strains must be alive to exert their anti-H. pylori activity, some lactobacilli strains are effective even when dead. One possible underlying mechanism of such an activity of non-living lactobacilli is reportedly co-aggregation with H. pylori. In this study, we found that a non-living heat-killed form of Lactobacillus johnsonii No.1088 (HK-LJ88) and also that of some other lactobacilli inhibited the growth of H. pylori in vitro. Furthermore, the number of H. pylori in the infected stomach of germ-free mice was significantly decreased by the repeated oral administration of HK-LJ88. Observation by scanning electron microscopy revealed that no co-aggregation had occurred between H. pylori and HK-LJ88; instead, deformations of H. pylori (e.g. disappearance of spiral, bending of cell body, coccoid formation, degradations, etc.) appeared after incubation for 24 h with HK-LJ88. These results suggest that HK-LJ88 inhibited H. pylori activity probably not by co-aggregation but by some unknown mechanism involving HK-LJ88's cell surface molecules and that even non-living lactobacilli are possibly useful to support H. pylori eradication therapy. Non-living heat-killed form of Lactobacillus johnsonii No.1088 was found to have anti-Helicobacter pylori activity not by the co-aggregation mechanism.

The internalization of Lactobacillus johnsonii N6.2 extracellular vesicles (EVs) by cells results in a significant induction of the 2’,5’-oligoadenylate synthetase (OAS) pathway. It also induces expression of IFI44L, MX1, MX2 and DDX60 . In this work, we evaluated whether the antiviral response induced by L. johnsonii N6.2-derived EVs, has an inhibitory effect on an RNA viral insult using murine norovirus (MNV-1) as the viral infection model. We found that RAW 264.7 Macrophages treated with EVs significantly decreased the levels of MNV-1 genome. These results were consistent with an increase in expression of Oas1b, Oas2, Oasl, Mx1, Mx2 and Ifi44l (6 hours post infection). Out of six proteins enriched in EVs, we found that SH3b2 domain of Sdp was the only protein effector molecule able to recapitulate the activation of the OAS pathway. In C57BL6 mice, the administration of live L. johnsonii N6.2, EVs, and Sdp-SH3b2/liposomes significantly decreased MNV-1 titers in the distal ileum, in contrast to the controls with PBS and liposomes alone that did not affect MNV-1. These results establish that the SH3b2 domain of Sdp, which is enriched in L. johnsonii derived EVs, is an effector molecule in EVs that can orchestrate the control of viral infections in vivo .

The trillions of microorganisms residing in the human body display varying degrees of compositional and functional diversities within and between individuals and contribute significantly to host physiology and susceptibility to disease. Microbial species present in the vaginal milieu of reproductive age women showed a large personal component and varies widely in different ethnic groups at the taxonomic, genomic, and functional levels. Lactobacillus iners, L. crispatus, L. gasseri, L. jensenii, and L. johnsonii are most frequently detected bacterial species in the vaginal milieu of reproductive age women. However, we currently lack (i) an understanding of the baseline vaginal microbiota of reproductive age Indian women, (ii) the extent of taxonomic and functional variations of vaginal microbiota between individuals and (iii) the genomic repertoires of the dominant vaginal microbiota associated with the Indian subjects. In our study, we analyzed the metagenome of high vaginal swab (HVS) samples collected from 40 pregnant Indian women enrolled in the GARBH-Ini cohort. Composition and abundance of bacterial species was characterized by pyrosequencing 16S rRNA gene. We identified 3067 OTUs with = 10 reads from four different bacterial phyla. Several species of lactobacilli were clustered into three community state types (CSTs). L. iners, L. crispatus, L. gasseri, and L. jensenii are the most frequently detected Lactobacillus species in the vaginal environment of Indian women. Other than Lactobacillus, several species of Halomonas were also identified in the vaginal environment of most of the women sampled. To gain genomic and functional insights, we isolated several Lactobacillus species from the HVS samples and explored their whole genome sequences by shotgun sequencing. We analyzed the genome of dominant Lactobacillus species, L. iners, L. crispatus, L. gasseri, and L. paragesseri to represent the CSTs and identify functions that may influence the composition of complex vaginal microbial ecology. This study reports for the first time the vaginal microbial ecology of Indian women and genomic insights into L. iners, L. crispatus, L. gasseri, and L. paragesseri commonly found in the genital tract of reproductive age women.

Three hundred and sixty presumptive lactic acid bacteria (LAB) isolated from pregnant sows, newborn, suckling, and weaned piglets were preliminarily screened for anti- Salmonella activity. Fifty-eight isolates consisting of Lactobacillus reuteri ( n  = 32), Lactobacillus salivarius ( n  = 10), Lactobacillus mucosae ( n  = 8), Lactobacillus johnsonii ( n  = 5), and Lactobacillus crispatus ( n  = 3) were selected and further characterized for probiotic properties including production of antimicrobial substances, acid and bile tolerance, and cell adherence to Caco-2 cells. Eight isolates including Lact. johnsonii LJ202 and Lact. reuteri LR108 were identified as potential probiotics. LJ202 was selected for further use in co-culture studies of two-bacterial and multiple-bacterial species to examine its inhibitory activity against Salmonella enterica serovar Enteritidis DMST7106 (SE7106). Co-culture of LJ202 and SE7106 showed that LJ202 could completely inhibit the growth of SE7106 in 10 h of co-culture. In co-culture of multiple-bacterial species, culturable fecal bacteria from pig feces were used as representative of multiple-bacterial species. The study was performed to examine whether interactions among multiple-bacterial species would influence antagonistic activity of LJ202 against SE7106 and fecal coliform bacteria. Co-culture of SE7106 with different combinations of fecal bacteria and probiotic (LJ202 and LR108) or non-probiotic ( Lact. mucosae LM303) strains revealed that the growth of SE7106 was completely inhibited either in the presence or in the absence of probiotic strains. Intriguingly, LJ202 exhibited notable inhibitory activity against fecal coliform bacteria while LR108 did not. Taken together, the results of co-culture studies suggested that LJ202 is a good probiotic candidate for further study its inhibitory effects against pathogen infections in pigs.