Role of meprins to protect ileal mucosa of Crohn's disease patients from colonization by adherent-invasive E. coli.

Ileal lesions in Crohn's disease (CD) patients are colonized by pathogenic adherent-invasive Escherichia coli (AIEC) able to adhere to and invade intestinal epithelial cells (IEC), and to survive within macrophages. The interaction of AIEC with IEC depends on bacterial factors mainly type 1 pil...

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Autores principales: Emilie Vazeille, Marie-Agnès Bringer, Aurélie Gardarin, Christophe Chambon, Christoph Becker-Pauly, Sylvia L F Pender, Christine Jakob, Stefan Müller, Daniel Lottaz, Arlette Darfeuille-Michaud
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Publicado: Public Library of Science (PLoS) 2011
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spelling oai:doaj.org-article:92c2861a920f4b86b717e5375019dc302021-11-18T06:51:57ZRole of meprins to protect ileal mucosa of Crohn's disease patients from colonization by adherent-invasive E. coli.1932-620310.1371/journal.pone.0021199https://doaj.org/article/92c2861a920f4b86b717e5375019dc302011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21698174/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Ileal lesions in Crohn's disease (CD) patients are colonized by pathogenic adherent-invasive Escherichia coli (AIEC) able to adhere to and invade intestinal epithelial cells (IEC), and to survive within macrophages. The interaction of AIEC with IEC depends on bacterial factors mainly type 1 pili, flagella, and outer membrane proteins. In humans, proteases can act as host defence mechanisms to counteract bacterial colonization. The protease meprin, composed of multimeric complexes of the two subunits alpha and beta, is abundantly expressed in IECs. Decreased levels of this protease correlate with the severity of the inflammation in patients with inflammatory bowel disease. The aim of the present study was to analyze the ability of meprin to modulate the interaction of AIEC with IECs. In patients with ileal CD we observed decreased levels of meprins, in particular that of meprin β. Dose-dependent inhibition of the abilities of AIEC strain LF82 to adhere to and invade intestinal epithelial T84 cells was observed when bacteria were pre-treated with both exogenous meprin α and meprin β. Dose-dependent proteolytic degradation of type 1 pili was observed in the presence of active meprins, but not with heat-inactivated meprins, and pretreatment of AIEC bacteria with meprins impaired their ability to bind mannosylated host receptors and led to decreased secretion of the pro-inflammatory cytokine IL-8 by infected T84 cells. Thus, decreased levels of protective meprins as observed in CD patients may contribute to increased AIEC colonization.Emilie VazeilleMarie-Agnès BringerAurélie GardarinChristophe ChambonChristoph Becker-PaulySylvia L F PenderChristine JakobStefan MüllerDaniel LottazArlette Darfeuille-MichaudPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 6, p e21199 (2011)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Emilie Vazeille
Marie-Agnès Bringer
Aurélie Gardarin
Christophe Chambon
Christoph Becker-Pauly
Sylvia L F Pender
Christine Jakob
Stefan Müller
Daniel Lottaz
Arlette Darfeuille-Michaud
Role of meprins to protect ileal mucosa of Crohn's disease patients from colonization by adherent-invasive E. coli.
description Ileal lesions in Crohn's disease (CD) patients are colonized by pathogenic adherent-invasive Escherichia coli (AIEC) able to adhere to and invade intestinal epithelial cells (IEC), and to survive within macrophages. The interaction of AIEC with IEC depends on bacterial factors mainly type 1 pili, flagella, and outer membrane proteins. In humans, proteases can act as host defence mechanisms to counteract bacterial colonization. The protease meprin, composed of multimeric complexes of the two subunits alpha and beta, is abundantly expressed in IECs. Decreased levels of this protease correlate with the severity of the inflammation in patients with inflammatory bowel disease. The aim of the present study was to analyze the ability of meprin to modulate the interaction of AIEC with IECs. In patients with ileal CD we observed decreased levels of meprins, in particular that of meprin β. Dose-dependent inhibition of the abilities of AIEC strain LF82 to adhere to and invade intestinal epithelial T84 cells was observed when bacteria were pre-treated with both exogenous meprin α and meprin β. Dose-dependent proteolytic degradation of type 1 pili was observed in the presence of active meprins, but not with heat-inactivated meprins, and pretreatment of AIEC bacteria with meprins impaired their ability to bind mannosylated host receptors and led to decreased secretion of the pro-inflammatory cytokine IL-8 by infected T84 cells. Thus, decreased levels of protective meprins as observed in CD patients may contribute to increased AIEC colonization.
format article
author Emilie Vazeille
Marie-Agnès Bringer
Aurélie Gardarin
Christophe Chambon
Christoph Becker-Pauly
Sylvia L F Pender
Christine Jakob
Stefan Müller
Daniel Lottaz
Arlette Darfeuille-Michaud
author_facet Emilie Vazeille
Marie-Agnès Bringer
Aurélie Gardarin
Christophe Chambon
Christoph Becker-Pauly
Sylvia L F Pender
Christine Jakob
Stefan Müller
Daniel Lottaz
Arlette Darfeuille-Michaud
author_sort Emilie Vazeille
title Role of meprins to protect ileal mucosa of Crohn's disease patients from colonization by adherent-invasive E. coli.
title_short Role of meprins to protect ileal mucosa of Crohn's disease patients from colonization by adherent-invasive E. coli.
title_full Role of meprins to protect ileal mucosa of Crohn's disease patients from colonization by adherent-invasive E. coli.
title_fullStr Role of meprins to protect ileal mucosa of Crohn's disease patients from colonization by adherent-invasive E. coli.
title_full_unstemmed Role of meprins to protect ileal mucosa of Crohn's disease patients from colonization by adherent-invasive E. coli.
title_sort role of meprins to protect ileal mucosa of crohn's disease patients from colonization by adherent-invasive e. coli.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/92c2861a920f4b86b717e5375019dc30
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