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Salmonella-induced mucosal lectin RegIII? kills competing gut microbiota.

ABSTRACT: Intestinal inflammation induces alterations of the gut microbiota and promotes overgrowth of the enteric pathogen Salmonella enterica by largely unknown mechanisms. Here, we identified a host factor involved in this process. Specifically, the C-type lectin RegIII? is strongly upregulated during mucosal infection and released into the gut lumen. In vitro, RegIII? kills diverse commensal gut bacteria but not Salmonella enterica subspecies I serovar Typhimurium (S. Typhimurium). Protection of the pathogen was attributable to its specific cell envelope structure. Co-infection experiments with an avirulent S. Typhimurium mutant and a RegIII?-sensitive commensal E. coli strain demonstrated that feeding of RegIII? was sufficient for suppressing commensals in the absence of all other changes inflicted by mucosal disease. These data suggest that RegIII? production by the host can promote S. Typhimurium infection by eliminating inhibitory gut microbiota.

SUBMITTER: Stelter C

PROVIDER: S-EPMC3111430 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature

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Salmonella-induced mucosal lectin RegIIIβ kills competing gut microbiota.

Stelter Christian C Käppeli Rina R König Claudia C Krah Alexander A Hardt Wolf-Dietrich WD Stecher Bärbel B Bumann Dirk D

PloS one 20110609 6

Intestinal inflammation induces alterations of the gut microbiota and promotes overgrowth of the enteric pathogen Salmonella enterica by largely unknown mechanisms. Here, we identified a host factor involved in this process. Specifically, the C-type lectin RegIIIβ is strongly upregulated during mucosal infection and released into the gut lumen. In vitro, RegIIIβ kills diverse commensal gut bacteria but not Salmonella enterica subspecies I serovar Typhimurium (S. Typhimurium). Protection of the p ...[more]

PMID: 21694778

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Project description:BackgroundSalmonella pullorum is one of the most harmful pathogens to avian species. Magnolol and honokiol, natural compounds extracted from Magnolia officinalis, exerts anti-inflammatory, anti-oxidant and antibacterial activities. This study was conducted to evaluate the effects of dietary supplemental magnolol and honokiol in broilers infected with S. pullorum. A total of 360 one-day-old broilers were selected and randomly divided into four groups with six replicates: the negative control group (CTL), S. pullorum-infected group (SP), and the S. pullorum-infected group supplemented with 300 mg/kg honokiol (SPH) or magnolol (SPM).ResultsThe results showed that challenging with S. pullorum impaired growth performance in broilers, as indicated by the observed decreases in body weight (P < 0.05) and average daily gains (P < 0.05), along with increased spleen (P < 0.01) and bursa of Fabricus weights (P < 0.05), serum globulin contents, and the decreased intestine villus height and villus/crypt ratios (P < 0.05). Notably, supplemental magnolol and honokiol attenuated these adverse changes, and the effects of magnolol were better than those of honokiol. Therefore, we performed RNA-Seq in ileum tissues and 16S rRNA gene sequencing of ileum bacteria. Our analysis revealed that magnolol increased the α-diversity (observed species, Chao1, ACE, and PD whole tree) and β-diversity of the ileum bacteria (P < 0.05). In addition, magnolol supplementation increased the abundance of Lactobacillus (P < 0.01) and decreased unidentified Cyanobacteria (P < 0.05) both at d 14 and d 21. Further study confirmed that differentially expressed genes induced by magnolol and honokiol supplementation enriched in cytokine-cytokine receptor interactions, in the intestinal immune network for IgA production, and in the cell adhesion molecule pathways.ConclusionsSupplemental magnolol and honokiol alleviated S. pullorum-induced impairments in growth performance, and the effect of magnolol was better than that of honokiol, which could be partially due to magnolol's ability to improve the intestinal microbial and mucosal barrier.

Project description:Salmonella is a foodborne pathogen that is one of the main causes of gastroenteric disease in humans and animals. As a natural organic substance, sodium humate (HNa) possesses antibacterial, antidiarrheal, and anti-inflammatory properties. However, it is unclear whether the HNa and HNa-derived microbiota exert alleviative effects on Salmonella enterica serovar Typhimurium-induced enteritis. We found that treatment with HNa disrupted the cell wall of S. Typhimurium and decreased the virulence gene expression. Next, we explored the effect of HNa presupplementation on S. Typhimurium-induced murine enteritis. The results revealed that HNa ameliorated intestinal pathological damage. In addition, we observed that presupplementation with HNa enhanced intestinal barrier function via modulating gut microbiota, downregulating toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) and NOD-like receptor protein 3 (NLRP3) signaling pathways, regulating intestinal mucosal immunity, and enhancing tight junction protein expression. To further validate the effect of HNa-derived microbiota on S. Typhimurium-induced enteritis, we performed fecal microbiota transplantation and found that HNa-derived microbiota also alleviated S. Typhimurium-induced intestinal damage. It is noteworthy that both HNa and HNa-derived microbiota improved the liver injury caused by S. Typhimurium infection. Collectively, this is the first study to confirm that HNa could alleviate S. Typhimurium-induced enteritis in a gut microbiota-dependent manner. This study provides a new perspective on HNa as a potential drug to prevent and treat salmonellosis. IMPORTANCE Salmonella Typhimurium is an important zoonotic pathogen, widely distributed in nature. S. Typhimurium is one of the leading causes of foodborne illnesses worldwide, and more than 350,000 people died from Salmonella infection each year, which poses a substantial risk to public health and causes a considerable economic loss. Here, we found that the S. Typhimurium infection caused severe intestinal and liver damage. In addition, we first found that sodium humate (HNa) and HNa-derived gut microbiota can alleviate S. Typhimurium infection-induced intestinal damage. These findings extend the knowledge about the public health risk and pathogenic mechanisms of S. Typhimurium.

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Salmonella-induced mucosal lectin RegIII? kills competing gut microbiota.

Publications

Salmonella-induced mucosal lectin RegIIIβ kills competing gut microbiota.

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