{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,11]],"date-time":"2026-11-11T08:24:39Z","timestamp":1794385479977,"version":"4.9.0"},"reference-count":33,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2006,1,1]],"date-time":"2006-01-01T00:00:00Z","timestamp":1136073600000},"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":[[2006,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Amebic liver abscess (ALA) is the most common extraintestinal manifestation of human infection by the enteric protozoan parasite\n                    <jats:italic>Entamoeba histolytica<\/jats:italic>\n                    . In contrast to intestinal infection, ALA greatly predominates in males but is rare in females. Since humans are the only relevant host for\n                    <jats:italic>E. histolytica<\/jats:italic>\n                    , experimental studies concerning this sexual dimorphism have been hampered by the lack of a suitable animal model. By serial liver passage of cultured\n                    <jats:italic>E. histolytica<\/jats:italic>\n                    trophozoites in gerbils and mice, we generated amebae which reproducibly induce ALA in C57BL\/6 mice. Interestingly, all animals developed ALA, but the time courses of abscess formation differed significantly between the genders. Female mice were able to clear the infection within 3 days, whereas in male mice the parasite could be recovered for at least 14 days. Accordingly, male mice showed a prolonged time of recovery from ALA. Immunohistology of abscesses revealed that polymorphonuclear leukocytes and macrophages were the dominant infiltrates, but in addition, \u03b3,\u03b4-T cells, NK cells, and natural killer T (NKT) cells were also present at early times during abscess development, whereas conventional \u03b1,\u03b2-T cells appeared later, when female mice had already cleared the parasite. Interestingly, male and female mice differed in early cytokine production in response to ameba infection. Enzyme-linked immunospot assays performed with spleen cells of infected animals revealed significantly higher numbers of interleukin-4-producing cells in male mice but significantly higher numbers of gamma interferon (IFN-\u03b3)-producing cells in female mice. Early IFN-\u03b3 production and the presence of functional NKT cells were found to be important for the control of hepatic amebiasis as application of an IFN-\u03b3-neutralizing monoclonal antibody or the use of NKT knockout mice (V\u03b114iNKT, J\u03b1 18\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) dramatically increased the size of ALA in female mice. In addition,\n                    <jats:italic>E. histolytica<\/jats:italic>\n                    trophozoites could be reisolated from liver abscesses of J\u03b118\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice on day 7 postinfection, when wild-type mice had already cleared the parasite. These data suggest that the sexual dimorphism in the control of ALA is due to gender-specific differences in early cytokine production mediated at least in part by NKT cells in response to\n                    <jats:italic>E. histolytica<\/jats:italic>\n                    infection of the liver.\n                  <\/jats:p>","DOI":"10.1128\/iai.74.1.118-124.2006","type":"journal-article","created":{"date-parts":[[2005,12,20]],"date-time":"2005-12-20T17:02:58Z","timestamp":1135098178000},"page":"118-124","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":92,"title":["Sexual Dimorphism in the Control of Amebic Liver Abscess in a Mouse Model of Disease"],"prefix":"10.1128","volume":"74","author":[{"given":"Hannelore","family":"Lotter","sequence":"first","affiliation":[{"name":"Department of Molecular Parasitology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Jacobs","sequence":"additional","affiliation":[{"name":"Department of Immunology, Bernhard Nocht Institute for Tropical Medicine, 20359 Hamburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Iris","family":"Gaworski","sequence":"additional","affiliation":[{"name":"Department of Immunology, Bernhard Nocht Institute for Tropical Medicine, 20359 Hamburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Egbert","family":"Tannich","sequence":"additional","affiliation":[{"name":"Department of Molecular Parasitology"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1572-0241.2000.01525.x"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.7538697"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/JCM.41.10.4745-4750.2003"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.4269\/ajtmh.2002.66.578"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/265341a0"},{"key":"e_1_3_2_7_2","first-page":"71","volume":"117","year":"1984","unstructured":"Chadee, K., and E. 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