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dc.rights.licenseopenen_US
dc.contributor.authorURIBE, Gabriela
dc.contributor.authorVILLEGER, Romain
hal.structure.identifierChimie et Biologie des Membranes et des Nanoobjets [CBMN]
dc.contributor.authorBRESSOLLIER, Philippe
dc.contributor.authorDILLARD, Rachel N.
dc.contributor.authorWORTHLEY, Daniel L.
dc.contributor.authorWANG, Timothy C.
dc.contributor.authorPOWELL, Don W.
hal.structure.identifierChimie et Biologie des Membranes et des Nanoobjets [CBMN]
dc.contributor.authorURDACI, Maria C.
ORCID: 0000-0002-0868-0050
IDREF: 033307679
dc.contributor.authorPINCHUK, Irina V.
dc.date.accessioned2020-04-08T12:39:07Z
dc.date.available2020-04-08T12:39:07Z
dc.date.issued2018
dc.identifier.otherhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6202218/bin/NIHMS974828-supplement-supplement_1.pdfen_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/4174
dc.description.abstractEnProstaglandin E2 (PGE2 ) plays a critical role in intestinal mucosal tolerance and barrier integrity. Cyclooxygenase-2 (COX-2)-dependent PGE2 production involves mobilization of arachidonic acid (AA). Lactobacillus rhamnosus GG (LbGG) is one of the most widely used probiotics reported to colonize the colonic mucosa. LbGG contributes to the protection of the small intestine against radiation injury through the repositioning of mucosal COX-2 expressing cells. However, it is unknown if LbGG modulates PGE2 production in the colonic mucosa under homeostasis and the major cellular elements involved in these processes. Colonic epithelial and CD90+ mesenchymal stromal cells, also known as (myo) fibroblasts (CMFs), are abundant innate immune cells in normal colonic mucosa able to produce PGE2 . Herein, we tested the hypothesis that under colonic mucosal homeostasis LbGG modulates the eicosanoid pathway resulting in increased PGE2 production in both epithelial and stromal cells. Among the five tested human colonic epithelial cell lines, only exposure of Caco-2 to LbGG for 24 h led to the mobilization of arachidonic acid (AA) with concomitant increase in the components within the leukotriene and COX-2 dependent PGE2 pathways. By contrast, CMFs isolated from the normal human colonic mucosa responded to LbGG with increased expression of COX-2 and PGE2 in the prostaglandin pathway, but not 5-LO in the leukotriene pathway. Oral gavage of C57BL/6 mice for 5 days with LbGG (5x108 CFU/dose) increased COX-2 expression in the colonic mucosa. The majority of cells upregulating COX-2 protein expression were located in the colonic lamina propria, and co-localized with alpha-SMA+ cells corresponding to the CMF phenotype. This process was MyD88 dependent, since silencing of MyD88 expression in CMFs abrogated LbGG-induced upregulation of COX-2 in culture and in vivo. Taken together, our data suggests that LbGG increases release of COX-2 mediated PGE2 , contributing to the maintenance of mucosal homeostasis in the colon and CMFs are among the major contributors to this process.
dc.language.isoENen_US
dc.subject.enlactic acid bacteria
dc.subject.enmechanism of action
dc.subject.enmetabolic processes
dc.subject.enmicrobial cell interaction
dc.subject.enCOX‐2
dc.title.enLactobacillus rhamnosus GG increases COX-2 expression and PGE2 secretion in colonic myofibroblasts via a MyD88-dependent mechanism during homeostasis
dc.title.alternativeCell Microbiol.en_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1111/cmi.12871
dc.subject.halChimie/Matériauxen_US
dc.identifier.pubmed29920917en_US
bordeaux.journalCellular microbiologyen_US
bordeaux.pagee12871-e12871en_US
bordeaux.volume20en_US
bordeaux.hal.laboratoriesInstitut de Chimie & de Biologie des Membranes & des Nano-objets (CBMN) - UMR 5248
bordeaux.issue11en_US
bordeaux.institutionBordeaux INPen_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-03160335
hal.version1
hal.date.transferred2021-03-05T09:17:55Z
hal.exporttrue
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