{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T12:57:33Z","timestamp":1791205053436,"version":"4.1.0"},"reference-count":23,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2007,12,1]],"date-time":"2007-12-01T00:00:00Z","timestamp":1196467200000},"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":[[2007,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Diseases associated with<jats:italic>Chlamydia<\/jats:italic>infection, such as pelvic inflammatory disease and ectopic pregnancy, are due to inflammation-mediated tissue damage and scarring that occur after chronic or repeated infections. The inflammatory chemokine interleukin-8 (IL-8) is produced by<jats:italic>Chlamydia<\/jats:italic>-infected cells through an endogenous mechanism of activation, independent of soluble factors in the supernatant. The host signaling pathways necessary for this response are not understood, but the mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase (ERK) has been shown to be activated at similar times as IL-8 mRNA up-regulation. The purpose of this study was to elucidate the MAPK pathways necessary to induce the endogenous IL-8 response to<jats:italic>Chlamydia trachomatis<\/jats:italic>infection of epithelial cells. IL-8 induced by infection with<jats:italic>C. trachomatis<\/jats:italic>L2 was shown to be dependent on ERK and independent of p38 and Jun N-terminal MAPK by use of chemical inhibitors of the signaling pathways. Persistent ERK activation during IL-8 mRNA production at 24 h postinfection was necessary to maintain the response.<jats:italic>C. trachomatis<\/jats:italic>serovar D also induced IL-8 in an ERK-dependent manner. We concluded that IL-8 induced during infection of epithelial cells is dependent on continual activation of ERK by<jats:italic>C. trachomatis<\/jats:italic>.<\/jats:p>","DOI":"10.1128\/iai.01029-07","type":"journal-article","created":{"date-parts":[[2007,9,25]],"date-time":"2007-09-25T00:34:31Z","timestamp":1190680471000},"page":"5924-5929","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":71,"title":["The Extracellular Signal-Regulated Kinase\/Mitogen-Activated Protein Kinase Pathway Induces the Inflammatory Factor Interleukin-8 following<i>Chlamydia trachomatis<\/i>Infection"],"prefix":"10.1128","volume":"75","author":[{"given":"Kerry R.","family":"Buchholz","sequence":"first","affiliation":[{"name":"Program in Infectious Diseases and Immunity"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard S.","family":"Stephens","sequence":"additional","affiliation":[{"name":"Program in Infectious Diseases and Immunity"},{"name":"the School of Public Health, University of California, Berkeley, 140 Warren Hall, Berkeley, California 94720"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1462-5822.2006.00747.x"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.70.6.3234-3248.2002"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1462-5822.2000.00058.x"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.20.091301.131133"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.61.11.4569-4574.1993"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M100609200"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.73.7.4017-4024.2005"},{"key":"e_1_3_2_9_2","first-page":"101","year":"1999","unstructured":"Hackstadt, T. 1999. 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