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Effects of Surfactant Protein‐A on the Interaction of Pneumocystis murina with its Host at Different Stages of the Infection in Mice
Author(s) -
LINKE MICHAEL J.,
ASHBAUGH ALAN A.,
KOCH JUDITH V.,
LEVIN LINDA,
TANAKA REIKO,
WALZER PETER D.
Publication year - 2009
Publication title -
journal of eukaryotic microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.067
H-Index - 77
eISSN - 1550-7408
pISSN - 1066-5234
DOI - 10.1111/j.1550-7408.2008.00363.x
Subject(s) - biology , heterologous , collectin , surfactant protein d , inoculation , microbiology and biotechnology , surfactant protein a , immune system , chemokine , pneumocystis carinii , homologous chromosome , host (biology) , immunology , pulmonary surfactant , innate immune system , pneumocystis jirovecii , biochemistry , human immunodeficiency virus (hiv) , ecology , gene
. We examined the effects of surfactant protein A (SP‐A), a collectin, on the interaction of Pneumocystis murina with its host at the beginning, early to middle, and late stages of infection. Pneumocystis murina from SP‐A wild‐type (WT) mice inoculated intractracheally into WT mice (WT S ‐WT R ) adhered well to alveolar macrophages, whereas organisms from SP‐A knockout (KO) mice inoculated into KO mice (KO S ‐KO R ) did not. Substitution of WT mice as the source of organisms (WT S ‐KO R ) or recipient host macrophages (KO S ‐WT R ) restored adherence to that found with WT S ‐WT R mice. In contrast, when immunosuppressed KO and WT mice were inoculated with P. murina from a homologous source (KO S ‐KO R , WT S ‐WT R ) or heterologous source (WT S ‐KO R , KO S ‐WT R ) and followed sequentially, WT S ‐KO R mice had the highest levels of infection at weeks 3 and 4; these mice also had the highest levels of the chemokine macrophage inflammatory protein‐2 and neutrophils in lavage fluid at week 3. Surfactant protein‐A administered to immunosuppressed KO S ‐KO R mice with Pneumocystis pneumonia for 8 wk as a therapeutic agent failed to lower the organism burden. We conclude that SP‐A can correct the host immune defect in the beginning of P. murina infection, but not in the middle or late stages of the infection.