{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T10:05:19Z","timestamp":1790762719166,"version":"4.1.0"},"reference-count":42,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2008,4,1]],"date-time":"2008-04-01T00:00:00Z","timestamp":1207008000000},"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":[[2008,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Helminths facilitate their own survival by actively modulating the immune systems of their hosts. We investigated the impacts that different life cycle stages of the rodent filaria<jats:italic>Litomosoides sigmodontis<\/jats:italic>have on the inflammatory responses of mice injected with sublethal doses of lipopolysaccharide (LPS). Mice infected with female adult worms from prepatent infections, worms which have not yet started to release microfilariae, developed lower levels of proinflammatory cytokines in the peripheral blood after LPS challenge than sham-treated controls, demonstrating that female adult worms can mitigate the innate immune response. The presence of microfilariae in mice, however, through either direct injection or implantation of microfilaria-releasing adult female worms, turned the LPS challenge fatal. This lethal outcome was characterized by increased plasma levels of gamma interferon (IFN-\u03b3), tumor necrosis factor alpha (TNF-\u03b1), interleukin 12 (IL-12), and IL-6, greater numbers of macrophages and granulocytes in the peripheral blood, and decreased body temperatures in microfilaria-infected mice. Microfilaria-infected mice deficient in IFN-\u03b3 receptor and TNF receptor 1 had increased survival rates after LPS challenge compared to immune-competent mice, suggesting that microfilariae worsen LPS-induced sepsis through actions of IFN-\u03b3 and TNF-\u03b1. In summary, we have demonstrated that infection of mice with<jats:italic>L. sigmodontis<\/jats:italic>female adult worms from prepatent infections protects mice injected with LPS whereas microfilariae worsen LPS-induced sepsis through the induction of proinflammatory cytokines and upregulation of granulocytes, NK cells, and monocytes in the peripheral blood.<\/jats:p>","DOI":"10.1128\/iai.01042-07","type":"journal-article","created":{"date-parts":[[2008,2,5]],"date-time":"2008-02-05T01:46:01Z","timestamp":1202175961000},"page":"1668-1677","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":15,"title":["Microfilariae of the Filarial Nematode<i>Litomosoides sigmodontis<\/i>Exacerbate the Course of Lipopolysaccharide-Induced Sepsis in Mice"],"prefix":"10.1128","volume":"76","author":[{"given":"Marc P.","family":"Hu\u0308bner","sequence":"first","affiliation":[{"name":"Institute of Tropical Medicine, University of Tu\u0308bingen, 72074 Tu\u0308bingen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bastian","family":"Pasche","sequence":"additional","affiliation":[{"name":"Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Svetoslav","family":"Kalaydjiev","sequence":"additional","affiliation":[{"name":"Institute for Medical Microbiology, Immunology, and Hygiene, Technical University of Munich, 81675 Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter T.","family":"Soboslay","sequence":"additional","affiliation":[{"name":"Institute of Tropical Medicine, University of Tu\u0308bingen, 72074 Tu\u0308bingen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Lengeling","sequence":"additional","affiliation":[{"name":"Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hartwig","family":"Schulz-Key","sequence":"additional","affiliation":[{"name":"Institute of Tropical Medicine, University of Tu\u0308bingen, 72074 Tu\u0308bingen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward","family":"Mitre","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wolfgang H.","family":"Hoffmann","sequence":"additional","affiliation":[{"name":"Institute of Tropical Medicine, University of Tu\u0308bingen, 72074 Tu\u0308bingen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1051\/parasite\/1994013241"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1067\/mai.2003.108"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V99.9.3427"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.micinf.2003.11.003"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1286-4579(00)01269-7"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1017\/S0022149X00028078"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.73.9.5468-5481.2005"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.176.1.472"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.175.12.8173"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature01326"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(01)06899-4"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1093\/intimm\/12.5.623"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1086\/426871"},{"key":"e_1_3_2_15_2","first-page":"259","volume":"52","year":"1983","unstructured":"Greene, B. 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