| First Author | Atochina EN | Year | 2004 |
| Journal | J Infect Dis | Volume | 189 |
| Issue | 8 | Pages | 1528-39 |
| PubMed ID | 15073692 | Mgi Jnum | J:90260 |
| Mgi Id | MGI:3042764 | Doi | 10.1086/383130 |
| Citation | Atochina EN, et al. (2004) Delayed clearance of pneumocystis carinii infection, increased inflammation, and altered nitric oxide metabolism in lungs of surfactant protein-D knockout mice. J Infect Dis 189(8):1528-39 |
| abstractText | 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. |
