{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Allen J"],"funding":["HHS | NIH | National Institute of Allergy and Infectious Diseases"],"pagination":["e00262-19"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6652777"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["87(8)"],"pubmed_abstract":["It has been shown that caspase-1, but not its upstream activator, ASC, contributes to oviduct pathology during mouse genital Chlamydia muridarum infection. We hypothesized that this dichotomy is due to the inadvertent absence of caspase-11 in previously used caspase-1-deficient mice. To address this, we studied the independent contributions of caspase-1 and -11 during genital Chlamydia infection. Our results show that caspase-11 deficiency was sufficient to recapitulate the effect of the combined absence of both caspase-1 and caspase-11 on oviduct pathology. Further, mice that were deficient for both caspase-1 and -11 but that expressed caspase-11 as a transgene (essentially, caspase-1-deficient mice) had no significant difference in oviduct pathology from control mice. Caspase-11-deficien"],"journal":["Infection and immunity"],"pubmed_title":["Caspase-11 Contributes to Oviduct Pathology during Genital Chlamydia Infection in Mice."],"pmcid":["PMC6652777"],"funding_grant_id":["AI067678"],"pubmed_authors":["Gyorke CE","Allen J","Tripathy MK","Zhang Y","Montgomery SA","Lovett A","Nagarajan UM"],"additional_accession":[]},"is_claimable":false,"name":"Caspase-11 Contributes to Oviduct Pathology during Genital Chlamydia Infection in Mice.","description":"It has been shown that caspase-1, but not its upstream activator, ASC, contributes to oviduct pathology during mouse genital Chlamydia muridarum infection. We hypothesized that this dichotomy is due to the inadvertent absence of caspase-11 in previously used caspase-1-deficient mice. To address this, we studied the independent contributions of caspase-1 and -11 during genital Chlamydia infection. Our results show that caspase-11 deficiency was sufficient to recapitulate the effect of the combined absence of both caspase-1 and caspase-11 on oviduct pathology. Further, mice that were deficient for both caspase-1 and -11 but that expressed caspase-11 as a transgene (essentially, caspase-1-deficient mice) had no significant difference in oviduct pathology from control mice. Caspase-11-deficien","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Aug","modification":"2025-04-04T21:27:58.479Z","creation":"2025-04-04T21:27:58.479Z"},"accession":"S-EPMC6652777","cross_references":{"pubmed":["31160363"],"doi":["10.1128/IAI.00262-19","10.1128/iai.00262-19"]}}