<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Allen J</submitter><funding>HHS | NIH | National Institute of Allergy and Infectious Diseases</funding><pagination>e00262-19</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6652777</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>87(8)</volume><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</pubmed_abstract><journal>Infection and immunity</journal><pubmed_title>Caspase-11 Contributes to Oviduct Pathology during Genital Chlamydia Infection in Mice.</pubmed_title><pmcid>PMC6652777</pmcid><funding_grant_id>AI067678</funding_grant_id><pubmed_authors>Gyorke CE</pubmed_authors><pubmed_authors>Allen J</pubmed_authors><pubmed_authors>Tripathy MK</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Montgomery SA</pubmed_authors><pubmed_authors>Lovett A</pubmed_authors><pubmed_authors>Nagarajan UM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Caspase-11 Contributes to Oviduct Pathology during Genital Chlamydia Infection in Mice.</name><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</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Aug</publication><modification>2025-04-04T21:27:58.479Z</modification><creation>2025-04-04T21:27:58.479Z</creation></dates><accession>S-EPMC6652777</accession><cross_references><pubmed>31160363</pubmed><doi>10.1128/IAI.00262-19</doi><doi>10.1128/iai.00262-19</doi></cross_references></HashMap>