{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T11:32:47Z","timestamp":1789990367137,"version":"4.0.1"},"reference-count":68,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2006,12,1]],"date-time":"2006-12-01T00:00:00Z","timestamp":1164931200000},"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":[[2006,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:italic>Campylobacter jejuni<\/jats:italic>\n            is a leading cause of human enterocolitis and is associated with postinfectious complications, including irritable bowel syndrome and Guillain-Barre\u0301 syndrome. However, the pathogenesis of\n            <jats:italic>C. jejuni<\/jats:italic>\n            infection remains poorly understood. Paracellular pathways in intestinal epithelial cells are gated by intercellular junctions (tight junctions and adherens junctions), providing a functional barrier between luminal microbes and host immune cells in the lamina propria. Here we describe alterations in tight junctions in intestinal epithelial monolayers following\n            <jats:italic>C. jejuni<\/jats:italic>\n            infection. Apical infection of polarized T84 monolayers caused a time-dependent decrease in transepithelial electrical resistance (TER). Immunofluorescence microscopy revealed a redistribution of the tight junctional transmembrane protein occludin from an intercellular to an intracellular location. Subcellular fractionation using equilibrium sucrose density gradients demonstrated decreased hyperphosphorylated occludin in lipid rafts, Triton X-100-soluble fractions, and the Triton X-100-insoluble pellet following apical infection. Apical infection with\n            <jats:italic>C. jejuni<\/jats:italic>\n            also caused rapid activation of NF-\u03baB and AP-1, phosphorylation of extracellular signal-regulated kinase, Jun N-terminal protein kinase, and p38 mitogen-activated protein kinases, and basolateral secretion of the CXC chemokine interleukin-8 (IL-8). Basolateral infection with\n            <jats:italic>C. jejuni<\/jats:italic>\n            caused a more rapid decrease in TER, comparable redistribution of tight-junction proteins, and secretion of more IL-8 than that seen with apical infection. These results suggest that compromised barrier function and increased chemokine expression contribute to the pathogenesis of\n            <jats:italic>C. jejuni<\/jats:italic>\n            -induced enterocolitis.\n          <\/jats:p>","DOI":"10.1128\/iai.00958-06","type":"journal-article","created":{"date-parts":[[2006,11,21]],"date-time":"2006-11-21T01:05:37Z","timestamp":1164071137000},"page":"6581-6589","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":167,"title":["Disruption of Tight Junctions and Induction of Proinflammatory Cytokine Responses in Colonic Epithelial Cells by\n            <i>Campylobacter jejuni<\/i>"],"prefix":"10.1128","volume":"74","author":[{"given":"Ming L.","family":"Chen","sequence":"first","affiliation":[{"name":"Division of Comparative Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhongming","family":"Ge","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James G.","family":"Fox","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine"},{"name":"Biological Engineering Division, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David B.","family":"Schauer","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine"},{"name":"Biological Engineering Division, Massachusetts Institute of Technology, Cambridge, Massachusetts 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