{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T04:28:49Z","timestamp":1775708929196,"version":"3.50.1"},"reference-count":49,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2010,1,1]],"date-time":"2010-01-01T00:00:00Z","timestamp":1262304000000},"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":[[2010,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Acute gonorrhea in women is characterized by a mucopurulent exudate that contains polymorphonuclear leukocytes (PMNs) with intracellular gonococci. Asymptomatic infections are also common. Information on the innate response to<jats:italic>Neisseria gonorrhoeae<\/jats:italic>in women is limited to studies with cultured cells, isolated immune cells, and analyses of cervicovaginal fluids. 17\u03b2-Estradiol-treated BALB\/c mice can be experimentally infected with<jats:italic>N. gonorrhoeae<\/jats:italic>, and a vaginal PMN influx occurs in 50 to 80% of mice. Here, we compared the colonization loads and proinflammatory responses of BALB\/c, C57BL\/6 and C3H\/HeN mice to<jats:italic>N. gonorrhoeae<\/jats:italic>. BALB\/c and C57BL\/6 mice were colonized at similar levels following inoculation with 10<jats:sup>6<\/jats:sup>CFU of<jats:italic>N. gonorrhoeae<\/jats:italic>. BALB\/c, but not C57BL\/6, mice exhibited a marked vaginal PMN influx. Tumor necrosis factor alpha, interleukin-6, macrophage inflammatory protein 2 (MIP-2), and keratinocyte-derived chemokine were elevated in vaginal secretions from infected BALB\/c mice, but not in those from C57BL\/6 mice. MIP-2 levels positively correlated with a vaginal PMN influx. In contrast to BALB\/c and C57BL\/6 mice, C3H\/HeN mice were resistant to infection, and there was no evidence of an inflammatory response. We conclude that<jats:italic>N. gonorrhoea<\/jats:italic>e causes a productive infection in BALB\/c mice that is characterized by the induction of proinflammatory cytokines and chemokines and the recruitment of PMNs. Infection of C57BL\/6 mice, in contrast, is more similar to asymptomatic infection. C3H\/HeN mice are inherently resistant to<jats:italic>N. gonorrhoeae<\/jats:italic>infection, and this resistance is not due to an overwhelming inflammatory response to infection. Host genetic factors can therefore impact susceptibility and the immune response to<jats:italic>N. gonorrhoeae<\/jats:italic>.<\/jats:p>","DOI":"10.1128\/iai.00711-09","type":"journal-article","created":{"date-parts":[[2009,11,10]],"date-time":"2009-11-10T02:44:45Z","timestamp":1257821085000},"page":"433-440","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":55,"title":["Mouse Strain-Dependent Differences in Susceptibility to<i>Neisseria gonorrhoeae<\/i>Infection and Induction of Innate Immune Responses"],"prefix":"10.1128","volume":"78","author":[{"given":"Mathanraj","family":"Packiam","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sandra J.","family":"Veit","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Deborah J.","family":"Anderson","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robin R.","family":"Ingalls","sequence":"additional","affiliation":[{"name":"Section of Infectious Diseases, Boston University School of Medicine, Boston, Massachusetts 02118"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ann E.","family":"Jerse","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/250353a0"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.8036519"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.2000.01694.x"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/169.3.532"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2334-6-90"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1462-5822.2009.01308.x"},{"key":"e_1_3_2_8_2","first-page":"13","volume":"40","year":"2001","unstructured":"Dalal, S. 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