Microbial induction of inflammatory bowel disease associated gene TL1A (TNFSF15) in antigen presenting cells Export

@article{citeulike:6009014, abstract = {TL1A is a member of the TNF superfamily and its expression is increased in the mucosa of inflammatory bowel disease patients. Neutralizing anti-mouse TL1A Ab attenuates chronic colitis in two T-cell driven murine models, suggesting that TL1A is a central modulator of gut mucosal inflammation in inflammatory bowel disease. We showed previously that TL1A is induced by immune complexes via the FcgammaR signaling pathway. In this study, we report that multiple bacteria, including gram negative organisms (E. coli, E. coli Nissle 1917, Salmonella typhimurium), gram positive organisms (Listeria monocytogenes, Staphylococcus epidermidis), partial anaerobes (Campylobacter jejuni), and obligate anaerobes (Bacteroides thetaiotaomicron, Bifidobacterium breve, Clostridium A4) activate TL1A expression in human APC, including monocytes and monocyte-derived DC. Bacterially induced TL1A mRNA expression correlates with the detection of TL1A protein levels. TL1A induced by bacteria is mediated in part by the TLR signaling pathway and inhibited by downstream blockade of p38 MAPK and NF-kappaB activation. Microbial induction of TL1A production by human APC potentiated CD4+ T-cell effector function by augmenting IFN-gamma production. Our findings suggest a role for TL1A in pro-inflammatory APC-T cell interactions and implicate TL1A in host responses to enteric microorganisms.}, address = {Inflammatory Bowel Disease Center and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Division of Gastroenterology, STAR Program, University of California Los Angeles, Los Angeles, CA, USA; Division of Gastroenterology and Hepatology, University of Alabama, Birmingham, AL, USA}, author = {Shih, David Q. and Kwan, Lola Y. and Chavez, Valerie and Cohavy, Offer and Gonsky, Rivkah and Chang, Elmer Y. and Chang, Christopher and Elson, Charles O. and Targan, Stephan R.}, citeulike-article-id = {6009014}, citeulike-linkout-0 = {http://dx.doi.org/10.1002/eji.200839087}, citeulike-linkout-1 = {http://www3.interscience.wiley.com/cgi-bin/abstract/122652589/ABSTRACT}, doi = {10.1002/eji.200839087}, issn = {1521-4141}, journal = {European Journal of Immunology}, keywords = {tlr, tnf-a}, number = {9999}, pages = {NA+}, posted-at = {2009-10-26 12:27:41}, priority = {3}, title = {Microbial induction of inflammatory bowel disease associated gene TL1A (TNFSF15) in antigen presenting cells}, url = {http://dx.doi.org/10.1002/eji.200839087}, volume = {9999}, year = {2009} }

TY - JOUR ID - citeulike:6009014 L3 - citeulike-article-id:6009014 N2 - TL1A is a member of the TNF superfamily and its expression is increased in the mucosa of inflammatory bowel disease patients. Neutralizing anti-mouse TL1A Ab attenuates chronic colitis in two T-cell driven murine models, suggesting that TL1A is a central modulator of gut mucosal inflammation in inflammatory bowel disease. We showed previously that TL1A is induced by immune complexes via the FcgammaR signaling pathway. In this study, we report that multiple bacteria, including gram negative organisms (E. coli, E. coli Nissle 1917, Salmonella typhimurium), gram positive organisms (Listeria monocytogenes, Staphylococcus epidermidis), partial anaerobes (Campylobacter jejuni), and obligate anaerobes (Bacteroides thetaiotaomicron, Bifidobacterium breve, Clostridium A4) activate TL1A expression in human APC, including monocytes and monocyte-derived DC. Bacterially induced TL1A mRNA expression correlates with the detection of TL1A protein levels. TL1A induced by bacteria is mediated in part by the TLR signaling pathway and inhibited by downstream blockade of p38 MAPK and NF-kappaB activation. Microbial induction of TL1A production by human APC potentiated CD4+ T-cell effector function by augmenting IFN-gamma production. Our findings suggest a role for TL1A in pro-inflammatory APC-T cell interactions and implicate TL1A in host responses to enteric microorganisms. IS - 9999 JF - European Journal of Immunology SN - 1521-4141 AD - Inflammatory Bowel Disease Center and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Division of Gastroenterology, STAR Program, University of California Los Angeles, Los Angeles, CA, USA; Division of Gastroenterology and Hepatology, University of Alabama, Birmingham, AL, USA TI - Microbial induction of inflammatory bowel disease associated gene TL1A (TNFSF15) in antigen presenting cells VL - 9999 SP - NA KW - tlr KW - tnf-a AU - Shih, David AU - Kwan, Lola AU - Chavez, Valerie AU - Cohavy, Offer AU - Gonsky, Rivkah AU - Chang, Elmer AU - Chang, Christopher AU - Elson, Charles AU - Targan, Stephan PY - 2009/// UR - http://dx.doi.org/10.1002/eji.200839087 ER -