{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T13:34:18Z","timestamp":1790948058699,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","license":[{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Virginia Tech Open Access Subvention Fund","award":["T32-OD010430"],"award-info":[{"award-number":["T32-OD010430"]}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["T32-OD010430"],"award-info":[{"award-number":["T32-OD010430"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2016]]},"abstract":"<jats:p><jats:italic>Toxoplasma gondii<\/jats:italic>is an obligate intracellular parasite that is the etiologic agent responsible for toxoplasmosis. Infection with<jats:italic>T. gondii<\/jats:italic>results in activation of nucleotide binding domain and leucine rich repeat containing receptors (NLRs). NLR activation leads to inflammasome formation, the activation of caspase-1, and the subsequent cleavage of IL-1<jats:italic>\u03b2<\/jats:italic>and IL-18. Recently, a noncanonical inflammasome has been characterized which functions through caspase-11 and appears to augment many biological functions previously considered to be dependent upon the canonical inflammasome. To better elucidate the function of this noncanonical inflammasome in toxoplasmosis, we utilized<jats:italic>Asc<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>and<jats:italic>Casp11<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice and infected these animals with<jats:italic>T. gondii<\/jats:italic>. Our data indicates that caspase-11 modulates the innate immune response to<jats:italic>T. gondii<\/jats:italic>through a mechanism which is distinct from that currently described for the canonical inflammasome.<jats:italic>Asc<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice demonstrated increased disease pathogenesis during the acute phase of<jats:italic>T. gondii<\/jats:italic>infection, whereas<jats:italic>Casp11<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice demonstrated significantly attenuated disease pathogenesis and reduced inflammation. This attenuated host response was associated with reduced local and systemic cytokine production, including diminished IL-1<jats:italic>\u03b2<\/jats:italic>. During the chronic phase of infection, caspase-11 deficiency resulted in increased neuroinflammation and tissue cyst burden in the brain. Together, our data suggest that caspase-11 functions to protect the host by enhancing inflammation during the early phase of infection in an effort to minimize disease pathogenesis during later stages of toxoplasmosis.<\/jats:p>","DOI":"10.1155\/2016\/9848263","type":"journal-article","created":{"date-parts":[[2016,6,9]],"date-time":"2016-06-09T22:03:14Z","timestamp":1465509794000},"page":"1-14","source":"Crossref","is-referenced-by-count":29,"title":["Caspase-11 Modulates Inflammation and Attenuates<i>Toxoplasma gondii<\/i>Pathogenesis"],"prefix":"10.1155","volume":"2016","author":[{"given":"Sheryl L.","family":"Coutermarsh-Ott","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John T.","family":"Doran","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences and 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