{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T21:30:54Z","timestamp":1788384654854,"version":"build-2803163510"},"reference-count":65,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2009,4,1]],"date-time":"2009-04-01T00:00:00Z","timestamp":1238544000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2009,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Gastrointestinal disease caused by\n            <jats:italic>Campylobacter jejuni<\/jats:italic>\n            is characterized by localized inflammation and the destruction of the epithelial cell barrier that forms host innate protection against pathogens. This can lead to an imbalance in fluid transport across the gastrointestinal tract, resulting in severe diarrhea. The mechanisms of host cell receptor recognition of\n            <jats:italic>C. jejuni<\/jats:italic>\n            and downstream immune signaling pathways leading to this inflammatory disease, however, remain unclear. The aim of this study was to analyze the mechanisms involved in\n            <jats:italic>C. jejuni<\/jats:italic>\n            induction of the acute-phase inflammatory response regulator interleukin-6 (IL-6). Polarized intestinal epithelial Caco-2 monolayers responded to infections with\n            <jats:italic>Salmonella enterica<\/jats:italic>\n            serovar Typhimurium and eight isolates of\n            <jats:italic>C. jejuni<\/jats:italic>\n            by an increase in levels of expression and secretion of IL-6. No such IL-6 response, however, was produced upon infection with the human commensal organism\n            <jats:italic>Lactobacillus rhamnosus<\/jats:italic>\n            GG. The IL-6 signaling pathway was further characterized using short interfering RNA complexes to block gene expression. The inhibition of myeloid differentiation primary response protein 88 (MyD88) expression in this manner did not affect\n            <jats:italic>C. jejuni<\/jats:italic>\n            -induced IL-6 secretion, suggesting a MyD88-independent route to IL-6 signal transduction in\n            <jats:italic>C. jejuni<\/jats:italic>\n            -infected human epithelial cells. However, a significant reduction in levels of IL-6 was evident in the absence of Toll-like receptor 2 (TLR-2) expression, implying a requirement for TLR-2 in\n            <jats:italic>C. jejuni<\/jats:italic>\n            recognition. Caco-2 cells were also treated with heat-inactivated and purified membrane components of\n            <jats:italic>C. jejuni<\/jats:italic>\n            to isolate the factor responsible for triggering IL-6 signaling. The results demonstrate that\n            <jats:italic>C. jejuni<\/jats:italic>\n            surface polysaccharides induce IL-6 secretion from intestinal epithelial cells via TLR-2 in a MyD88-independent manner.\n          <\/jats:p>","DOI":"10.1128\/iai.00707-08","type":"journal-article","created":{"date-parts":[[2009,1,13]],"date-time":"2009-01-13T01:58:57Z","timestamp":1231811937000},"page":"1553-1560","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":49,"title":["<i>Campylobacter jejuni<\/i>\n            Drives MyD88-Independent Interleukin-6 Secretion via Toll-Like Receptor 2"],"prefix":"10.1128","volume":"77","author":[{"given":"Lorna M.","family":"Friis","sequence":"first","affiliation":[{"name":"Department of Medical Microbiology and Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Monika","family":"Keelan","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, University of Alberta, 1-63 Medical Sciences Building, Edmonton T6G 2H7, Alberta, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diane E.","family":"Taylor","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology and Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80596-8"},{"key":"e_1_3_2_3_2","first-page":"1","volume":"311","year":"2006","unstructured":"Akira, S. 2006. 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