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J Med Microbiol 55 (2006), 143-147; DOI: 10.1099/jmm.0.46190-0
© 2006 Society for General Microbiology
ISSN 0022-2615

Efficient resolution of Pneumocystis murina infection in surfactant protein A-deficient mice following withdrawal of corticosteroid-induced immunosuppression

Michael Linke1,2, Alan Ashbaugh2, Judith Koch2, Reiko Tanaka2 and Peter Walzer1,2

1 Department of Veterans Affairs Medical Center, Research Service, 3200 Vine St, Cincinnati, OH 45220, USA

2 University of Cincinnati College of Medicine, Department of Internal Medicine, Division of Infectious Diseases, 231 Bethesda, Cincinnati, OH 45221, USA

Correspondence
Michael Linke
Michael.Linke{at}med.va.gov

Received 5 June 2005
Accepted 7 October 2005

Following withdrawal of immunosuppression, surfactant protein A (SP-A)-deficient and wild-type mice cleared Pneumocystis murina infection in a similar manner, but exhibited significant differences in lymphocyte populations, interleukin (IL)-6 levels and chemokine expression levels. A higher percentage of lymphocytes were detected in lung lavage fluid from SP-A-deficient mice, but more CD4+ T cells were isolated from lung tissue of wild-type mice. Higher concentrations of IL-6 were detected in lavage fluid and enhanced expression of lymphotactin and RANTES were detected in the lungs of wild-type mice. Equal levels of surfactant protein D were detected in SP-A-deficient and wild-type mice and no differences were detected in markers of lung injury between the two strains of mice. Thus, SP-A does not enhance organism clearance, but does modulate the host immune response during resolution of P. murina infection.

Abbreviations: DEX, dexamethasone; Ltn, lymphotactin; PcP, Pneumocystis pneumonia; RPA, ribonuclease protection assay; SP-A, surfactant protein A; SP-D, surfactant protein D.






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