ArticleInfection and immunity2001
Role for inducible nitric oxide synthase in protection from chronic Chlamydia trachomatis urogenital disease in mice and its regulation by oxygen free radicals.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 68 citations in OpenAlex.
- Identification of collaborative cross mouse strains susceptible to chlamydial induction of hydrosalpinx.Infection and immunity · 2026Article
- Pathogenic and Protective Roles of Neutrophils inPathogens (Basel, Switzerland) · 2025Review
- Immunopathogenesis of genital Chlamydia infection: insights from mouse models.Pathogens and disease · 2021Review
- NK Cell-Mediated Processing Of Chlamydia psittaci Drives Potent Anti-Bacterial Th1 Immunity.Scientific reports · 2019Article
- Chlamydial Plasmid-Dependent Pathogenicity.Trends in microbiology · 2017Review
- Sensing the enemy, containing the threat: cell-autonomous immunity to Chlamydia trachomatis.FEMS microbiology reviews · 2016Review
- iNOS-dependent sweating and eNOS-dependent cutaneous vasodilation are evident in younger adults, but are diminished in older adults exercising in the heat.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Article
- Complement factor C5 but not C3 contributes significantly to hydrosalpinx development in mice infected with Chlamydia muridarum.Infection and immunity · 2014Article
- Lack of long-lasting hydrosalpinx in A/J mice correlates with rapid but transient chlamydial ascension and neutrophil recruitment in the oviduct following intravaginal inoculation with Chlamydia muridarum.Infection and immunity · 2014Article
- Immunity, immunopathology, and human vaccine development against sexually transmitted Chlamydia trachomatis.Human vaccines & immunotherapeutics · 2014Review
- Article
- Perforin-2 restricts growth of Chlamydia trachomatis in macrophages.Infection and immunity · 2013Article
- Article
- Enhanced neutrophil longevity and recruitment contribute to the severity of oviduct pathology during Chlamydia muridarum infection.Infection and immunity · 2011Article
- Nitric oxide synthases and tubal ectopic pregnancies induced by Chlamydia infection: basic and clinical insights.Molecular human reproduction · 2010Review
- Pathogenesis of genital tract disease due to Chlamydia trachomatis.The Journal of infectious diseases · 2010Review
- Role of activins and inducible nitric oxide in the pathogenesis of ectopic pregnancy in patients with or without Chlamydia trachomatis infection.Clinical and vaccine immunology : CVI · 2009Article
- Temporal delay of peak T-cell immunity determines Chlamydia pneumoniae pulmonary disease in mice.Infection and immunity · 2008Article
- Caspase-1 contributes to Chlamydia trachomatis-induced upper urogenital tract inflammatory pathologies without affecting the course of infection.Infection and immunity · 2008Article
- Characterization of an acid-dependent arginine decarboxylase enzyme from Chlamydophila pneumoniae.Journal of bacteriology · 2007Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
It has been previously reported that although inducible nitric oxide synthase (iNOS) gene knockout (NOS2(-/-)) mice resolve Chlamydia trachomatis genital infection, the production of reactive nitrogen species (RNS) via iNOS protects a significant proportion of mice from hydrosalpinx formation and infertility. We now report that higher in vivo RNS production correlates with mouse strain-related innate resistance to hydrosalpinx formation. We also show that mice with a deletion of a key component of phagocyte NADPH oxidase (p47(phox-/-)) resolve infection, produce greater amounts of RNS in vivo, and sustain lower rates of hydrosalpinx formation than both wild-type (WT) NOS2(+/+) and NOS2(-/-) controls. When we induced an in vivo chemical block in iNOS activity in p47(phox-/-) mice using N(G)-monomethyl-L-arginine (L-NMMA), a large proportion of these mice eventually succumbed to opportunistic infections, but not before they resolved their chlamydial infections. Interestingly, when compared to WT and untreated p47(phox-/-) controls, L-NMMA-treated p47(phox-/-) mice resolved their infections more rapidly. However, L-NMMA-treated p47(phox-/-) mice lost resistance to chronic chlamydial disease, as evidenced by an increased rate of hydrosalpinx formation that was comparable to that for NOS2(-/-) mice. We conclude that phagocyte oxidase-derived reactive oxygen species (ROS) regulate RNS during chlamydial urogenital infection in the mouse. We further conclude that while neither phagocyte oxidase-derived ROS nor iNOS-derived RNS are essential for resolution of infection, RNS protect from chronic chlamydial disease in this model.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.