{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T23:04:02Z","timestamp":1793315042618,"version":"4.5.0"},"reference-count":40,"publisher":"Springer Science and Business Media LLC","issue":"1","content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Gut Pathog"],"published-print":{"date-parts":[[2009,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Campylobacter<\/jats:italic>\n                      enteritis represents a risk factor for the development of inflammatory bowel disease (IBD) via unknown mechanisms. As IBD patients exhibit inflammatory responses to their commensal intestinal microflora, factors that induce translocation of commensal bacteria across the intestinal epithelium may contribute to IBD pathogenesis. This study sought to determine whether\n                      <jats:italic>Campylobacter<\/jats:italic>\n                      induces translocation of non-invasive intestinal bacteria, and characterize underlying mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Mice were infected with\n                      <jats:italic>C. jejuni<\/jats:italic>\n                      and translocation of intestinal bacteria was assessed by quantitative bacterial culture of mesenteric lymph nodes (MLNs), liver, and spleen. To examine mechanisms of\n                      <jats:italic>Campylobacter<\/jats:italic>\n                      -induced bacterial translocation, transwell-grown T84 monolayers were inoculated with non-invasive\n                      <jats:italic>Escherichia coli<\/jats:italic>\n                      HB101 \u00b1 wild-type\n                      <jats:italic>Campylobacter<\/jats:italic>\n                      or invasion-defective mutants, and bacterial internalization and translocation were measured. Epithelial permeability was assessed by measuring flux of a 3 kDa dextran probe. The role of lipid rafts was assessed by cholesterol depletion and caveolin co-localization.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>C. jejuni<\/jats:italic>\n                      81\u2013176 induced translocation of commensal intestinal bacteria to the MLNs, liver, and spleen of infected mice. In T84 monolayers,\n                      <jats:italic>Campylobacter<\/jats:italic>\n                      -induced internalization and translocation of\n                      <jats:italic>E. coli<\/jats:italic>\n                      occurred via a transcellular pathway, without increasing epithelial permeability, and was blocked by depletion of epithelial plasma membrane cholesterol. Invasion-defective mutants and\n                      <jats:italic>Campylobacter<\/jats:italic>\n                      -conditioned cell culture medium also induced\n                      <jats:italic>E. coli<\/jats:italic>\n                      translocation, indicating that\n                      <jats:italic>C. jejuni<\/jats:italic>\n                      does not directly 'shuttle' bacteria into enterocytes. In\n                      <jats:italic>C. jejuni<\/jats:italic>\n                      -treated monolayers, translocating\n                      <jats:italic>E. coli<\/jats:italic>\n                      associated with lipid rafts, and this phenomenon was blocked by cholesterol depletion.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Campylobacter<\/jats:italic>\n                      , regardless of its own invasiveness, promotes the translocation of non-invasive bacteria across the intestinal epithelium via a lipid raft-mediated transcellular process.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/1757-4749-1-2","type":"journal-article","created":{"date-parts":[[2009,2,3]],"date-time":"2009-02-03T14:39:42Z","timestamp":1233671982000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":115,"title":["Campylobacter jejuni induces transcellular translocation of commensal bacteria via lipid rafts"],"prefix":"10.1186","volume":"1","author":[{"given":"Lisa D","family":"Kalischuk","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G Douglas","family":"Inglis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andre G","family":"Buret","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2009,2,3]]},"reference":[{"issue":"Suppl 1","key":"2_CR1","doi-asserted-by":"publisher","first-page":"S16","DOI":"10.1097\/00054725-200402001-00004","volume":"10","author":"F Shanahan","year":"2004","unstructured":"Shanahan F: Host-flora interactions in inflammatory bowel disease. 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