Delayed clearance of Pneumocystis carinii infection, increased inflammation, and altered nitric oxide metabolism in lungs of surfactant protein-D knockout mice

Elena N. Atochina, Andrew J. Gow, James M. Beck, Angela Franciska Haczku, Adam Inch, Helchem Kadire, Yaniv Tomer, Christine Davis, Angela M. Preston, Francis R Poulain, Samuel Hawgood, Michael F. Beers

Research output: Contribution to journalArticle

58 Scopus citations

Abstract

Surfactant protein-D (SP-D), a member of the "collectin" family, has been shown to play a role in innate immunity through modulation of inflammation and clearance of organisms. The role of SP-D in host defense against Pneumocystis carinii pneumonia was assessed using SP-D knockout (KO) mice. When inoculated with P. carinii, both wild-type (wt) and SP-D KO mice required CD4 cell depletion to develop infection. In CD4 cell-depleted models, 2 weeks after infection with P. carinii, SP-D KO mice developed increased intensity of infection, compared with wt mice, despite higher lung-inflammation scores and increased amounts of alveolar inflammatory cells. The increased inflammation seen in SP-D KO mice was accompanied by increases in lung weight, expression of inducible nitric oxide (NO) synthase, total NO levels, and 3-nitrotyrosine levels in lung tissue. These results indicate that SP-D plays a role in host defense against P. carinii in vivo by modulating clearance of organisms, lung inflammation, and metabolism of NO.

Original languageEnglish (US)
Pages (from-to)1528-1539
Number of pages12
JournalJournal of Infectious Diseases
Volume189
Issue number8
DOIs
StatePublished - Apr 15 2004
Externally publishedYes

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Immunology

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