scholarly journals Neither Interleukin-6 nor Inducible Nitric Oxide Synthase Is Required for Clearance of Chlamydia trachomatis from the Murine Genital Tract Epithelium

1998 ◽  
Vol 66 (3) ◽  
pp. 1265-1269 ◽  
Author(s):  
Linda L. Perry ◽  
Karen Feilzer ◽  
Harlan D. Caldwell
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Chlamydia Trachomatis ◽  
Immune Responses ◽  
Inducible Nitric Oxide Synthase ◽  
Interleukin 6 ◽  
Vaginal Infection ◽  
Th1 Cytokine ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

ABSTRACT Female mice bearing targeted mutations in the interleukin-6 or inducible nitric oxide synthase locus mounted effective immune responses following vaginal infection with Chlamydia trachomatis. Chlamydial clearance rates, local Th1 cytokine production, and host antibody responses were similar to those of immunocompetent control mice. Therefore, neither gene product appears to be critical for the resolution of chlamydial infections of the urogenital epithelium.

Altered immune responses in mice lacking inducible nitric oxide synthase

Nature ◽  
1995 ◽  
Vol 375 (6530) ◽  
pp. 408-411 ◽  
Author(s):  
Xiao-qing Wei ◽  
Ian G. Charles ◽  
Austin Smith ◽  
Jan Ure ◽  
Gui-jie Feng ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Immune Responses ◽  
Inducible Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals Chlamydia trachomatis Persistence in the Female Mouse Genital Tract: Inducible Nitric Oxide Synthase and Infection Outcome

2001 ◽  
Vol 69 (8) ◽  
pp. 5131-5137 ◽  
Author(s):  
Kyle H. Ramsey ◽  
Gurwattan S. Miranpuri ◽  
Ira M. Sigar ◽  
Scott Ouellette ◽  
Gerald I. Byrne
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Chlamydia Trachomatis ◽  
Inducible Nitric Oxide Synthase ◽  
Genital Tract ◽  
Lung Fibroblasts ◽  
Inos Activity ◽  
Ifn Γ ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

ABSTRACT It was previously reported that female mice resolve a primaryChlamydia trachomatis urogenital infection independent of inducible nitric oxide synthase (iNOS). We now report that although iNOS-deficient (NOS2−/−) mice resolve culture-apparent infection in a fashion similar to that of normal control (NOS2 +/+) mice, they sustain significantly increased rates of disease, as assessed by hydrosalpinx formation. PCR amplification of ompAfollowed by Southern blot detection of amplicands revealed the presence of chlamydial DNA in the lower genital tracts of both NOS2−/− and NOS2 +/+ mice at ≥120 days postinfection and in upper genital tract tissues at >120 days postinfection. However, only NOS2−/− mice shed low numbers of viable chlamydiae from the lower genital tract after immunosuppressive treatment at 120 days postinfection. When cultured primary murine lung fibroblasts were activated in the presence of gamma interferon (IFN-γ), inhibition of chlamydial growth occurred in both NOS2 +/+ and NOS2−/− cells, but the inhibition was reversible after removal of the cytokine in the NOS2−/− primary cell culture only. The iNOS-independent inhibition was microbistatic but was independent of 2,3-indoleamine dioxygenase activity. We conclude that chlamydial DNA and antigens persist in mice subsequent to culture-apparent resolution. In addition, IFN-γ induces in vivo inhibition of chlamydial growth through microbistatic mechanisms in the absence of iNOS activity, but in the presence of iNOS activity, IFN-γ is microbicidal and effects eradication.

scholarly journals Adjuvant Immunotherapy Is Dependent on Inducible Nitric Oxide Synthase

2001 ◽  
Vol 193 (11) ◽  
pp. 1261-1268 ◽  
Author(s):  
Daniel A. Kahn ◽  
D. Clay Archer ◽  
Daniel P. Gold ◽  
Carolyn J. Kelly
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Immune Responses ◽  
Inducible Nitric Oxide Synthase ◽  
Interferon Γ ◽  
Type I ◽  
Freund’S Adjuvant ◽  
Freund's Adjuvant ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Rodents immunized with complete Freund's adjuvant (CFA) are resistant to subsequent attempts to induce autoimmune disease, while animals immunized with incomplete Freund's adjuvant (IFA) remain susceptible. Mycobacterial extracts can stimulate inducible nitric oxide synthase (NOS2) gene transcription. Robust expression of NOS2 has been linked to suppression of T cell proliferation and alterations in immune responses. Our studies investigated the hypothesis that the immunoprotective effect of CFA before immunization requires functional NOS2. NOS2 gene expression is chronically elevated in lymph nodes and spleens of CFA-immunized mice. Maximal expression of NOS2 after CFA immunization requires the presence of functional type I tumor necrosis factor α receptor (TNFR1) and interferon γ. Groups of nontreated and CFA-preimmunized male C57BL/6J or C57BL/6NOS2−/− mice were immunized with myelin oligodendrocyte glycoprotein (MOG) peptide 35–55 in CFA to induce experimental allergic encephalomyelitis (EAE). Wild-type C57BL/6J mice were protected from the development of symptoms of EAE, while the NOS2−/− mice failed to be protected. NOS2-dependent effects of CFA included an augmentation of the MOG-specific IgG1 response, a decrease in interleukin 6 production by MOG-reactive lymphocytes, and a marked decrease in mononuclear cell infiltrates in the central nervous system. These studies support the hypothesis that CFA immunization modulates immune responses through a nitric oxide–dependent mechanism.

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