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Lactobacillus fermentum attenuates the proinflammatory effect of Yersinia enterocolitica on human epithelial cells

Background: Lactobacilli represent a major component of the human microbiota. In this study we investigated whether and how Lactobacillus fermentum inhibits the proinflammatory responses of human epithelial cells on Yersinia enterocolitica infection. Methods: Human epithelial cells were exposed to Y...

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Published in:Inflammatory bowel diseases 2007-01, Vol.13 (1), p.83-90
Main Authors: Frick, Julia‐Stefanie, Schenk, Katrin, Quitadamo, Matteo, Kahl, Frauke, Köberle, Martin, Bohn, Erwin, Aepfelbacher, Martin, Autenrieth, Ingo B.
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cited_by cdi_FETCH-LOGICAL-c3909-277f718904e77c01494ad335a30e94ea3674faf783e3f094b34d4187ce3da4483
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container_title Inflammatory bowel diseases
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creator Frick, Julia‐Stefanie
Schenk, Katrin
Quitadamo, Matteo
Kahl, Frauke
Köberle, Martin
Bohn, Erwin
Aepfelbacher, Martin
Autenrieth, Ingo B.
description Background: Lactobacilli represent a major component of the human microbiota. In this study we investigated whether and how Lactobacillus fermentum inhibits the proinflammatory responses of human epithelial cells on Yersinia enterocolitica infection. Methods: Human epithelial cells were exposed to Y. enterocolitica pYV− or L. fermentum or to both strains, combinations of heat‐killed L. fermentum or supernatant of L. fermentum cultures and Y. enterocolitica. The modulation of Y. enterocolitica induced IL‐8 levels in the culture supernatants was determined and activation of Rac, p38, and NF‐κB was investigated. Results: Exposure of human epithelial cells to L. fermentum does not induce NF‐κB activation and subsequent IL‐8 secretion in HeLa cells, whereas Y. enterocolitica induces NF‐κB activation and high levels of IL‐8. Viable L. fermentum, supernatant of L. fermentum cultures, but not heat‐killed L. fermentum, inhibited IL‐8 secretion of HeLa cells triggered by Y. enterocolitica. Lactobacillus fermentum‐exposed HeLa cells showed decreased Rac, p38, and NF‐κB activation after Y. enterocolitica infection. Treatment of L. fermentum supernatants with phospholipase C abolished the inhibitory effect, indicating that a secreted phospholipid mediates the antiinflammatory properties of L. fermentum. Adhesion to or invasion of Y. enterocolitica into epithelial cells was not altered by coincubation with L. fermentum. Conclusion: Our results lead to the conclusion that L. fermentum inhibits the Y. enterocolitica‐induced IL‐8 production by a possibly secreted phospholipid of
doi_str_mv 10.1002/ibd.20009
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In this study we investigated whether and how Lactobacillus fermentum inhibits the proinflammatory responses of human epithelial cells on Yersinia enterocolitica infection. Methods: Human epithelial cells were exposed to Y. enterocolitica pYV− or L. fermentum or to both strains, combinations of heat‐killed L. fermentum or supernatant of L. fermentum cultures and Y. enterocolitica. The modulation of Y. enterocolitica induced IL‐8 levels in the culture supernatants was determined and activation of Rac, p38, and NF‐κB was investigated. Results: Exposure of human epithelial cells to L. fermentum does not induce NF‐κB activation and subsequent IL‐8 secretion in HeLa cells, whereas Y. enterocolitica induces NF‐κB activation and high levels of IL‐8. Viable L. fermentum, supernatant of L. fermentum cultures, but not heat‐killed L. fermentum, inhibited IL‐8 secretion of HeLa cells triggered by Y. enterocolitica. Lactobacillus fermentum‐exposed HeLa cells showed decreased Rac, p38, and NF‐κB activation after Y. enterocolitica infection. Treatment of L. fermentum supernatants with phospholipase C abolished the inhibitory effect, indicating that a secreted phospholipid mediates the antiinflammatory properties of L. fermentum. Adhesion to or invasion of Y. enterocolitica into epithelial cells was not altered by coincubation with L. fermentum. Conclusion: Our results lead to the conclusion that L. fermentum inhibits the Y. enterocolitica‐induced IL‐8 production by a possibly secreted phospholipid of &lt;10 kDa molecular weight. These data suggest that L. fermentum may have probiotic properties modulating intestinal inflammatory responses and might offer new therapeutic strategies in the treatment of intestinal inflammatory diseases. 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In this study we investigated whether and how Lactobacillus fermentum inhibits the proinflammatory responses of human epithelial cells on Yersinia enterocolitica infection. Methods: Human epithelial cells were exposed to Y. enterocolitica pYV− or L. fermentum or to both strains, combinations of heat‐killed L. fermentum or supernatant of L. fermentum cultures and Y. enterocolitica. The modulation of Y. enterocolitica induced IL‐8 levels in the culture supernatants was determined and activation of Rac, p38, and NF‐κB was investigated. Results: Exposure of human epithelial cells to L. fermentum does not induce NF‐κB activation and subsequent IL‐8 secretion in HeLa cells, whereas Y. enterocolitica induces NF‐κB activation and high levels of IL‐8. Viable L. fermentum, supernatant of L. fermentum cultures, but not heat‐killed L. fermentum, inhibited IL‐8 secretion of HeLa cells triggered by Y. enterocolitica. Lactobacillus fermentum‐exposed HeLa cells showed decreased Rac, p38, and NF‐κB activation after Y. enterocolitica infection. Treatment of L. fermentum supernatants with phospholipase C abolished the inhibitory effect, indicating that a secreted phospholipid mediates the antiinflammatory properties of L. fermentum. Adhesion to or invasion of Y. enterocolitica into epithelial cells was not altered by coincubation with L. fermentum. Conclusion: Our results lead to the conclusion that L. fermentum inhibits the Y. enterocolitica‐induced IL‐8 production by a possibly secreted phospholipid of &lt;10 kDa molecular weight. These data suggest that L. fermentum may have probiotic properties modulating intestinal inflammatory responses and might offer new therapeutic strategies in the treatment of intestinal inflammatory diseases. 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Lactobacillus fermentum‐exposed HeLa cells showed decreased Rac, p38, and NF‐κB activation after Y. enterocolitica infection. Treatment of L. fermentum supernatants with phospholipase C abolished the inhibitory effect, indicating that a secreted phospholipid mediates the antiinflammatory properties of L. fermentum. Adhesion to or invasion of Y. enterocolitica into epithelial cells was not altered by coincubation with L. fermentum. Conclusion: Our results lead to the conclusion that L. fermentum inhibits the Y. enterocolitica‐induced IL‐8 production by a possibly secreted phospholipid of &lt;10 kDa molecular weight. These data suggest that L. fermentum may have probiotic properties modulating intestinal inflammatory responses and might offer new therapeutic strategies in the treatment of intestinal inflammatory diseases. 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subjects Bacterial Adhesion
Cell culture
Cells, Cultured
Culture Media, Conditioned
Data processing
Endopeptidase K - pharmacology
Epithelial cells
Epithelial Cells - metabolism
Epithelial Cells - microbiology
Glycerophospholipids - chemistry
Glycerophospholipids - pharmacology
HeLa Cells
Humans
IL‐8
Infection
Inflammation
Inflammation Mediators - metabolism
Inflammatory bowel diseases
Inflammatory diseases
Interleukin 8
Interleukin-8 - secretion
Intestine
Iron Compounds - pharmacology
Lactobacilli
Lactobacillus
Lactobacillus fermentum
Lactobacillus fermentum - physiology
Molecular weight
NF- Kappa B protein
NF-kappa B - metabolism
p38 Mitogen-Activated Protein Kinases - metabolism
Phospholipase C
Phospholipids
probiotics
rac1 GTP-Binding Protein - metabolism
Yersinia
Yersinia enterocolitica
Yersinia enterocolitica - pathogenicity
Yersinia Infections - metabolism
title Lactobacillus fermentum attenuates the proinflammatory effect of Yersinia enterocolitica on human epithelial cells
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