English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Pneumocystis carinii pneumonia remains a serious complication for immunocompromised patients. In the present study,P. carinii organisms interacted with gamma interferon (IFN-γ)-stimulated alveolar macrophages (AMs) to activate thel -arginine-dependent cytocidal pathway involving reactive nitrogen intermediates (RNI) that were assayed as nitrite (NO2 − ). Unstimulated cultures of AMs produced negligible quantities of RNI. Addition ofP. carinii organisms to IFN-γ-primed AMs resulted in greatly enhanced production of RNI. NO2 − levels increased from 0.8 ± 0.4 to 11.1 ± 3.8 μM as early as 6 h afterP. carinii organisms were incubated with IFN-γ-stimulated AMs and to 35.1 ± 8.9 μM after a 24-h incubation, a near-maximum level. High levels of NO2 − were produced by AMs primed with as little as 10 U of IFN-γ per ml in the presence ofP. carinii , and a 20-fold increase in IFN-γ concentration resulted in only a further 65% increase in NO2 − production. RNI-dependent killing ofP. carinii was demonstrated by both a51 Cr release assay and a [35 S]methionine pulse immunoprecipitation assay. Addition of either monoclonal tumor necrosis factor alpha (TNF-α) neutralizing antibody or 200 μMN G -monomethyl-l -arginine (l -N G MMA), a competitive inhibitor of thel -arginine-dependent pathway, significantly decreased NO2 − production and reducedP. carinii killing. TNF-α alone had no effect onP. carinii viability. These results suggest that (i) the specific interaction ofP. carinii organisms with IFN-γ-primed AMs triggers the production of RNI, (ii) RNI are toxic toP. carinii , and (iii) TNF-α likely plays a central role in mediatingP. carinii killing by IFN-γ-stimulated AMs.

infection and immunity

Gamma Interferon Stimulates Rat Alveolar Macrophages To Kill<i>Pneumocystis carinii</i>by<scp>l</scp>-Arginine- and Tumor Necrosis Factor-Dependent Mechanisms

Gamma Interferon Stimulates Rat Alveolar Macrophages To KillPneumocystis cariniibyl-Arginine- and Tumor Necrosis Factor-Dependent Mechanisms