{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T17:48:40Z","timestamp":1761155320209},"reference-count":27,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2010,3,1]],"date-time":"2010-03-01T00:00:00Z","timestamp":1267401600000},"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":[[2010,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            To define the roles of specific complement activation pathways in host defense against\n            <jats:italic>Streptococcus pneumoniae<\/jats:italic>\n            in acute otitis media (AOM), we investigated the susceptibility to AOM in mice deficient in complement factor B and C2 (\n            <jats:italic>Bf\/C2<\/jats:italic>\n            <jats:sup>\u2212\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            ), C1qa (\n            <jats:italic>C1qa<\/jats:italic>\n            <jats:sup>\u2212\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            ), and factor B (\n            <jats:italic>Bf<\/jats:italic>\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            ). Bacterial titers of both\n            <jats:italic>S. pneumoniae<\/jats:italic>\n            serotype 6A and 14 in the middle ear lavage fluid samples from\n            <jats:italic>Bf\/C2<\/jats:italic>\n            <jats:sup>\u2212\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            ,\n            <jats:italic>Bf<\/jats:italic>\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            , and\n            <jats:italic>C1qa<\/jats:italic>\n            <jats:sup>\u2212\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            mice were significantly higher than in samples from wild-type mice 24 h after transtympanical infection (\n            <jats:italic>P<\/jats:italic>\n            &lt; 0.05) and remained persistently higher in samples from\n            <jats:italic>Bf\/C2<\/jats:italic>\n            <jats:sup>\u2212\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            mice than in samples from wild-type mice. Bacteremia occurred in\n            <jats:italic>Bf\/C2<\/jats:italic>\n            <jats:sup>\u2212\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            ,\n            <jats:italic>Bf<\/jats:italic>\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            , and\n            <jats:italic>C1qa<\/jats:italic>\n            <jats:sup>\u2212\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            mice infected with both strains, but not in wild-type mice. Recruitment of inflammatory cells was paralleled by enhanced production of inflammatory mediators in the middle ear lavage samples from\n            <jats:italic>Bf\/C2<\/jats:italic>\n            <jats:sup>\u2212\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            mice. C3b deposition on both strains was greatest for sera obtained from wild-type mice, followed by\n            <jats:italic>C1qa<\/jats:italic>\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            and\n            <jats:italic>Bf<\/jats:italic>\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            mice, and least for\n            <jats:italic>Bf\/C2<\/jats:italic>\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>\/<\/jats:sup>\n            <jats:sup>\u2212<\/jats:sup>\n            mice. Opsonophagocytosis and whole-blood killing capacity of both strains were significantly decreased in the presence of sera or whole blood from complement-deficient mice compared to wild-type mice. These findings indicate that both the classical and alternative complement pathways are critical for middle ear immune defense against\n            <jats:italic>S. pneumoniae<\/jats:italic>\n            . The reduced capacity of complement-mediated opsonization and phagocytosis in the complement-deficient mice appears to be responsible for the impaired clearance of\n            <jats:italic>S. pneumoniae<\/jats:italic>\n            from the middle ear and dissemination to the bloodstream during AOM.\n          <\/jats:p>","DOI":"10.1128\/iai.01012-09","type":"journal-article","created":{"date-parts":[[2010,1,12]],"date-time":"2010-01-12T02:44:53Z","timestamp":1263264293000},"page":"976-983","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":27,"title":["Enhanced Susceptibility to Acute Pneumococcal Otitis Media in Mice Deficient in Complement C1qa, Factor B, and Factor B\/C2"],"prefix":"10.1128","volume":"78","author":[{"given":"Hua Hua","family":"Tong","sequence":"first","affiliation":[{"name":"Department of Otolaryngology, College of Medicine and Public Health, The Ohio State University, Columbus, Ohio 43210"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yong Xing","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Otolaryngology, College of Medicine and Public Health, The Ohio State University, Columbus, Ohio 43210"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gregory L.","family":"Stahl","sequence":"additional","affiliation":[{"name":"Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Harvard Institutes of Medicine, Harvard Medical School, Boston, Massachusetts 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joshua M.","family":"Thurman","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Colorado Denver School of Medicine, Aurora, Colorado 80045"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.32.1.311-317.1981"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/ng0598-56"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.180.6.4124"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.012669199"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0002950"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.71.1.211-217.2003"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.molimm.2008.06.021"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1177\/00034894941030S516"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.73.7.4245-4252.2005"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.3109\/inf.1981.13.issue-3.04"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.heares.2006.05.012"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.16.8720"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.01186-08"},{"key":"e_1_3_2_15_2","first-page":"279","year":"1987","unstructured":"Mogi, G., and J. 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