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National Institute of Environmental Health Sciences

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Publication Detail

Title: Caspase-11 Contributes to Oviduct Pathology during Genital Chlamydia Infection in Mice.

Authors: Allen 4th, John; Gyorke, Clare E; Tripathy, Manoj K; Zhang, Yugen; Lovett, Angela; Montgomery, Stephanie A; Nagarajan, Uma M

Published In Infect Immun, (2019 08)

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-deficient mice showed reduced dilation in both the oviducts and uterus. To determine the mechanism by which caspase-11-deficient mice developed reduced pathology, the chlamydial burden and immune cell infiltration were determined in the oviducts. In the caspase-11-deficient mice, we observed increased chlamydial burdens in the upper genital tract, which correlated with increased CD4 T cell recruitment, suggesting a contribution of caspase-11 in infection control. Additionally, there were significantly fewer neutrophils in the oviducts of caspase-11-deficient mice, supporting the observed decrease in the incidence of oviduct pathology. Therefore, caspase-11 activation contributes to pathogen control and oviduct disease independently of caspase-1 activation.

PubMed ID: 31160363 Exiting the NIEHS site

MeSH Terms: Animals; Caspase 1/physiology; Caspases/genetics; Caspases/physiology*; Chlamydia Infections/pathology*; Female; Mice; Mice, Inbred C57BL; Neutrophil Infiltration; Oviducts/pathology*; Reproductive Tract Infections/pathology*

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