Affiliation:
1. Critical Care Medicine Department, NIH Clinical Center, National Institutes of Health, Bethesda, Maryland, USA
Abstract
ABSTRACT
Pneumocystis
remains an important pathogen of immunosuppressed patients, causing a potentially life-threatening pneumonia. Despite its medical importance, the immune responses required to control infection, including the role of interleukin-17 (IL-17), which is important in controlling other fungal infections, have not been clearly defined. Using flow cytometry and intracellular cytokine staining after stimulation with phorbol myristate acetate and ionomycin, we examined gamma interferon (IFN-γ), IL-4, IL-5, and IL-17 production by lung lymphocytes in immunocompetent C57BL/6 mice over time following infection with
Pneumocystis
murina
. We also examined the clearance of
Pneumocystis
infection in IL-17A-deficient mice. The production of both IFN-γ and IL-17 by pulmonary lymphocytes increased during infection, with maximum production at approximately days 35 to 40, coinciding with peak
Pneumocystis
levels in the lungs, while minimal changes were seen in IL-4- and IL-5-positive cells. The proportion of cells producing IFN-γ was consistently higher than for cells producing IL-17, with peak levels of ∼25 to 30% of CD3
+
T cells for the former compared to ∼15% for the latter. Both CD4
+
T cells and γδ T cells produced IL-17. Administration of anti-IFN-γ antibody led to a decrease in IFN-γ-positive cells, and an increase in IL-5-positive cells, but did not impact clearance of
Pneumocystis
infection. Despite the increases in IL-17 production during infection, IL-17A-deficient mice cleared
Pneumocystis
infection with kinetics similar to C57BL/6 mice. Thus, while IL-17 production in the lungs is increased during
Pneumocystis
infection in immunocompetent mice, IL-17A is not required for control of
Pneumocystis
infection.
Funder
HHS | NIH | NIH Clinical Center
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
11 articles.
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