ArticleInfection and immunity2008
Caspase-1 contributes to Chlamydia trachomatis-induced upper urogenital tract inflammatory pathologies without affecting the course of infection.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed, 131 citations in OpenAlex.
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- A study on the association between gut microbiota, inflammation, and type 2 diabetes.Applied microbiology and biotechnology · 2024Article
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- Preclinical screen for protection efficacy of chlamydial antigens that are immunogenic in humans.Infection and immunity · 2023Article
- IL-23 receptor signaling licenses group 3-like innate lymphoid cells to restrict a live-attenuated oral Chlamydia vaccine in the gut.Infection and immunity · 2023Article
- Gut dysbiosis contributes to chlamydial induction of hydrosalpinx in the upper genital tract.Frontiers in microbiology · 2023Article
- Evidence for cGAS-STING Signaling in the Female Genital Tract Resistance to Chlamydia trachomatis Infection.Infection and immunity · 2022Article
- Characterization of Pathogenic CD8Infection and immunity · 2022Article
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- Immunopathogenesis of genital Chlamydia infection: insights from mouse models.Pathogens and disease · 2021Review
- Host cell death during infection with Chlamydia: a double-edged sword.FEMS microbiology reviews · 2021Review
- Neurodegenerative Disease and the NLRP3 Inflammasome.Frontiers in pharmacology · 2021Review
- Effects of Immunomodulatory Drug Fingolimod (FTY720) onInfection and immunity · 2020Article
- Suppression of Chlamydial Pathogenicity by Nonspecific CD8Infection and immunity · 2020Article
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- Gastrointestinal Coinfection Promotes Chlamydial Pathogenicity in the Genital Tract.Infection and immunity · 2020Article
- The Cryptic Plasmid ImprovesInfection and immunity · 2020Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chlamydia trachomatis infection induces inflammatory pathologies in the upper genital tract, potentially leading to ectopic pregnancy and infertility in the affected women. Caspase-1 is required for processing and release of the inflammatory cytokines interleukin-1beta (IL-1beta), IL-18, and possibly IL-33. In the present study, we evaluated the role of caspase-1 in chlamydial infection and pathogenesis. Although chlamydial infection induced caspase-1 activation and processing of IL-1beta, mice competent and mice deficient in caspase-1 experienced similar courses of chlamydial infection in their urogenital tracts, suggesting that Chlamydia-activated caspase-1 did not play a significant role in resolution of chlamydial infection. However, when genital tract tissue pathologies were examined, the caspase-1-deficient mice displayed much reduced inflammatory damage. The reduction in inflammation was most obvious in the fallopian tube tissue. These observations demonstrated that although caspase-1 is not required for controlling chlamydial infection, caspase-1-mediated responses can exacerbate the Chlamydia-induced inflammatory pathologies in the upper genital tract, suggesting that the host caspase-1 may be targeted for selectively attenuating chlamydial pathogenicity without affecting the host defense against chlamydial infection.
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