{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T10:47:25Z","timestamp":1783594045726,"version":"3.55.0"},"reference-count":58,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2014,8,1]],"date-time":"2014-08-01T00:00:00Z","timestamp":1406851200000},"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":[[2014,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Hydrosalpinx is a pathological hallmark of tubal infertility associated with chlamydial infection. However, the mechanisms of hydrosalpinx remain unknown. Here, we report that complement factor 5 (C5) contributes significantly to chlamydial induction of hydrosalpinx. Mice lacking C5 (C5<jats:sup>\u2212\/\u2212<\/jats:sup>) failed to develop any hydrosalpinx, while \u223c42% of the corresponding wild-type mice (C5<jats:sup>+\/+<\/jats:sup>) did so following intravaginal infection with<jats:named-content content-type=\"genus-species\">Chlamydia muridarum<\/jats:named-content>. Surprisingly, deficiency in C3 (C3<jats:sup>\u2212\/\u2212<\/jats:sup>), an upstream component of the complement system, did not affect mouse susceptibility to chlamydial induction of hydrosalpinx. Interestingly, C5 activation was induced by chlamydial infection in oviducts of C3<jats:sup>\u2212\/\u2212<\/jats:sup>mice, explaining why the C3<jats:sup>\u2212\/\u2212<\/jats:sup>mice remained susceptible to chlamydial induction of hydrosalpinx. Similar levels of live chlamydial organisms were recovered from oviduct tissues of both C5<jats:sup>\u2212\/\u2212<\/jats:sup>and C5<jats:sup>+\/+<\/jats:sup>mice, suggesting that C5 deficiency did not affect<jats:named-content content-type=\"genus-species\">C. muridarum<\/jats:named-content>ascending infection. Furthermore, C5<jats:sup>\u2212\/\u2212<\/jats:sup>mice were still more resistant to hydrosalpinx induction than C5<jats:sup>+\/+<\/jats:sup>mice, even when live<jats:named-content content-type=\"genus-species\">C. muridarum<\/jats:named-content>organisms were directly delivered into the upper genital tract, both confirming the role of C5 in promoting hydrosalpinx and indicating that the C5-facilitated hydrosalpinx was not due to enhancement of ascending infection. The C5<jats:sup>\u2212\/\u2212<\/jats:sup>mice displayed significantly reduced lumenal inflammatory infiltration and cytokine production in oviduct tissue, suggesting that C5 may contribute to chlamydial induction of hydrosalpinx by enhancing inflammatory responses.<\/jats:p>","DOI":"10.1128\/iai.01833-14","type":"journal-article","created":{"date-parts":[[2014,5,20]],"date-time":"2014-05-20T07:56:29Z","timestamp":1400572589000},"page":"3154-3163","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":42,"title":["Complement Factor C5 but Not C3 Contributes Significantly to Hydrosalpinx Development in Mice Infected with Chlamydia muridarum"],"prefix":"10.1128","volume":"82","author":[{"given":"Zhangsheng","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, 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