ArticleAmerican journal of respiratory cell and molecular biology2011
Defective nitric oxide production by alveolar macrophages during Pneumocystis pneumonia.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Immune responses of different hosts toEuropean respiratory review : an official journal of the European Respiratory Society · 2025Review
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- Increased susceptibility to pneumonia due to tumour necrosis factor inhibition and prospective immune system rescueFrontiers in cellular and infection microbiology · 2022Review
- Article
- Fatal Cytomegalovirus Infection in an Adult with Inherited NOS2 Deficiency.The New England journal of medicine · 2020Article
- Mechanisms of Action of Vitamin D as Supplemental Therapy for Pneumocystis Pneumonia.Antimicrobial agents and chemotherapy · 2017Article
- Differential Macrophage Polarization from Pneumocystis in Immunocompetent and Immunosuppressed Hosts: Potential Adjunctive Therapy during Pneumonia.Infection and immunity · 2017Article
- Classical versus alternative macrophage activation: the Ying and the Yang in host defense against pulmonary fungal infections.Mucosal immunology · 2014Review
- All-trans retinoic acid in combination with primaquine clears pneumocystis infection.PloS one · 2013Article
- Adjunctive corticosteroids in non-HIV immunocompromised patients withTherapeutic advances in infectious diseaseArticle
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The effect of nitric oxide (NO) on Pneumocystis (Pc) organisms, the role of NO in the defense against infection with Pc, and the production of NO by alveolar macrophages (AMs) during Pneumocystis pneumonia (PCP) were investigated. The results indicate that NO was toxic to Pc organisms and inhibited their proliferation in culture. When the production of NO was inhibited by intraperitoneal injection of rats with the nitric oxide synthase inhibitor L-N(5)-(1-iminoethyl) ornithine, progression of Pc infection in immunocompetent rats was enhanced. Concentrations of NO in bronchoalveolar lavage fluids from immunosuppressed, Pc-infected rats and mice were greatly reduced, compared with those from uninfected animals, and AMs from these animals were defective in NO production. However, inducible nitric oxide synthase (iNOS) mRNA and protein concentrations were high in AMs from Pc-infected rats and mice. Immunoblot analysis showed that iNOS in AMs from Pc-infected rats existed primarily as a monomer, but the homo-dimerization of iNOS monomers was required for the production of NO. When iNOS dimerization cofactors, including calmodulin, were added to macrophage lysates, iNOS dimerization increased, whereas incubation of the same lysates with all cofactors except calmodulin did not rescue iNOS dimer formation. These data suggest that NO is important in the defense against Pc infection, but that the production of NO in AMs during PCP is defective because of the reduced dimerization of iNOS.
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