{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T23:08:49Z","timestamp":1791328129883,"version":"4.3.1"},"reference-count":49,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2014,5,1]],"date-time":"2014-05-01T00:00:00Z","timestamp":1398902400000},"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":[[2014,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Helminth infections affect 1 billion people worldwide and render these individuals susceptible to bacterial coinfection through incompletely understood mechanisms. This includes urinary tract coinfection by bacteria and<jats:named-content content-type=\"genus-species\">Schistosoma haematobium<\/jats:named-content>worms, the etiologic agent of urogenital schistosomiasis. To study the mechanisms of<jats:named-content content-type=\"genus-species\">S. haematobium<\/jats:named-content>-bacterial urinary tract coinfections, we combined the first tractable model of urogenital schistosomiasis with an established mouse model of bacterial urinary tract infection (UTI). A single bladder exposure to<jats:named-content content-type=\"genus-species\">S. haematobium<\/jats:named-content>eggs triggers interleukin-4 (IL-4) production and makes BALB\/c mice susceptible to bacterial UTI when they are otherwise resistant. Ablation of IL-4 receptor alpha (IL-4R\u03b1) signaling restored the baseline resistance of BALB\/c mice to bacterial UTI despite prior exposure to<jats:named-content content-type=\"genus-species\">S. haematobium<\/jats:named-content>eggs. Interestingly, numbers of NKT cells were decreased in coexposed versus bacterially monoinfected bladders. Given that schistosome-induced, non-natural killer T (NKT) cell leukocyte infiltration may dilute NKT cell numbers in the bladders of coexposed mice without exerting a specific functional effect on these cells, we next examined NKT cell biology on a per-cell basis. Invariant NKT (iNKT) cells from coexposed mice expressed less gamma interferon (IFN-\u03b3) per cell than did those from mice with UTI alone. Moreover, coexposure resulted in lower CD1d expression in bladder antigen-presenting cells (APC) than did bacterial UTI alone in an IL-4R\u03b1-dependent fashion. Finally, coexposed mice were protected from prolonged bacterial infection by administration of \u03b1-galactosylceramide, an iNKT cell agonist. Our findings point to a previously unappreciated role for helminth-induced IL-4 in impairment of iNKT cell-mediated clearance of bacterial coexposure.<\/jats:p>","DOI":"10.1128\/iai.01578-13","type":"journal-article","created":{"date-parts":[[2014,3,19]],"date-time":"2014-03-19T04:09:28Z","timestamp":1395202168000},"page":"2087-2097","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":36,"title":["Helminth-Induced Interleukin-4 Abrogates Invariant Natural Killer T Cell Activation-Associated Clearance of Bacterial Infection"],"prefix":"10.1128","volume":"82","author":[{"given":"Yi-Ju","family":"Hsieh","sequence":"first","affiliation":[{"name":"Department of Urology, Stanford University School of Medicine, Stanford University, Stanford, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chi-Ling","family":"Fu","sequence":"additional","affiliation":[{"name":"Department of Urology, Stanford University School of Medicine, Stanford University, Stanford, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael H.","family":"Hsieh","sequence":"additional","affiliation":[{"name":"Department of Urology, Stanford University School of Medicine, Stanford University, Stanford, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0001-706X(03)00029-9"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/B978-0-12-391429-3.00005-8"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.chom.2012.10.001"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri843"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1067\/mda.2003.7"},{"key":"e_1_3_2_7_2","first-page":"103","article-title":"Urinary schistosomiasis and concomitant urinary tract pathogens among school children in metropolitan Ibadan","volume":"5","author":"Adeyeba OA","year":"2002","unstructured":"AdeyebaOAOjeagaSGT. 2002. 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