Data from: Irgm proteins attenuate inflammatory disease in mouse models of genital Chlamydia infection

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  • Chlamydiae are obligate intracellular bacterial pathogens that may cause genital pathology via induction of destructive host immune responses. Human-adapted Chlamydia trachomatis causes inflammatory disease in human hosts but is easily cleared in mice, and mouse-adapted Chlamydia muridarum establishes a productive and pathogenic infection in murine hosts. While numerous anti-chlamydial host resistance factors have been discovered in mice and humans alike, little is known about host factors promoting host fitness independent of host resistance. Here, we show that interferon-inducible immunity-related GTPase M (Irgm) proteins function as such host factors ameliorating infection-associated sequalae in the murine female genital tract, thus characterizing Irgm proteins as mediators of disease tolerance. Specifically, we demonstrate that mice deficient for all three murine Irgm paralogs (pan-Irgm−/−) are defective for cell-autonomous immunity to C. trachomatis, which correlates with an early and transient increase in bacterial burden and sustained hyperinflammation in vivo. In contrast, upon infection of pan-Irgm−/− mice with C. muridarum, bacterial burden is unaffected, yet genital inflammation and scarring pathology are nonetheless increased, demonstrating that Irgm proteins can promote host fitness without altering bacterial burden. Additionally, pan-Irgm−/− mice display increased granulomatous inflammation in genital Chlamydia infection, implicating Irgm proteins in the regulation of granuloma formation and maintenance. These findings demonstrate that Irgm proteins regulate pathogenic immune responses to Chlamydia infection in vivo, establishing an effective infection model to examine the immunoregulatory functions and mechanisms of Irgm proteins. ... [Read More]

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Data Citation
  • Dockterman, J., Reitano, J. R., Everitt, J. I., Wallace, G. D., Hendrix, M., Taylor, G. A., & Coers, J. (2024). Data from: Irgm proteins attenuate inflammatory disease in mouse models of genital Chlamydia infection. Duke Research Data Repository. https://doi.org/10.7924/r4r214s79
DOI
  • 10.7924/r4r214s79
Publication Date
ARK
  • ark:/87924/r4r214s79
Type
Related Materials
Funding Agency
  • National Institute of Allergy and Infectious Disease
Grant Number
  • AI103197
Title
  • Data from: Irgm proteins attenuate inflammatory disease in mouse models of genital Chlamydia infection
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