scholarly journals 120-kD surface glycoprotein of Pneumocystis carinii is a ligand for surfactant protein A.

1992 ◽  
Vol 89 (1) ◽  
pp. 143-149 ◽  
Author(s):  
P E Zimmerman ◽  
D R Voelker ◽  
F X McCormack ◽  
J R Paulsrud ◽  
W J Martin
Keyword(s):  
Pneumocystis Carinii ◽  
Protein A ◽  
Surfactant Protein ◽  
Surface Glycoprotein ◽  
Surfactant Protein A

scholarly journals Enhanced Lung Injury and Delayed Clearance of Pneumocystis carinii in Surfactant Protein A-Deficient Mice: Attenuation of Cytokine Responses and Reactive Oxygen-Nitrogen Species

2004 ◽  
Vol 72 (10) ◽  
pp. 6002-6011 ◽  
Author(s):  
Elena N. Atochina ◽  
James M. Beck ◽  
Angela M. Preston ◽  
Angela Haczku ◽  
Yaniv Tomer ◽  
...  
Keyword(s):  
Lung Injury ◽  
Pneumocystis Carinii ◽  
Protein A ◽  
Reactive Oxygen ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Interleukin 4 ◽  
Nitrogen Species ◽  
Cell Counts ◽  
Deficient Mice

ABSTRACT Surfactant protein A (SP-A), a member of the collectin family, selectively binds to Pneumocystis carinii and mediates interactions between pathogen and host alveolar macrophages in vitro. To test the hypothesis that mice lacking SP-A have delayed clearance of Pneumocystis organisms and enhanced lung injury, wild-type C57BL/6 (WT) and SP-A-deficient mice (SP-A−/−) with or without selective CD4+-T-cell depletion were intratracheally inoculated with Pneumocystis organisms. Four weeks later, CD4-depleted SP-A-deficient mice had developed a more severe Pneumocystis infection than CD4-depleted WT (P. carinii pneumonia [PCP] scores of 3 versus 2, respectively). Whereas all non-CD4-depleted WT mice were free of PCP, intact SP-A−/− mice also had evidence of increased organism burden. Pneumocystis infection in SP-A-deficient mice was associated histologically with enhanced peribronchial and/or perivascular cellularity (score of 4 versus 2, SP-A−/− versus C57BL/6 mice, respectively) and a corresponding increase in bronchoalveolar lavage (BAL) cell counts. Increases in SP-D content, gamma interferon, interleukin-4, interleukin-5, and tumor necrosis factor alpha in BAL fluid occurred but were attenuated in PCP-infected SP-A−/− mice compared to WT mice. There were increases in total BAL NO levels in both infected groups, but nitrite levels were higher in SP-A−/− mice, indicating a reduction in production of higher oxides of nitrogen that was also reflected in lower levels of 3-nitrotyrosine staining in the SP-A−/− group. We conclude that despite increases in inflammatory cells, SP-A-deficient mice infected with P. carinii exhibit an enhanced susceptibility to the organism and attenuated production of proinflammatory cytokines and reactive oxygen-nitrogen species. These data support the concept that SP-A is a local effector molecule in the lung host defense against P. carinii in vivo.

scholarly journals Surfactant protein-A levels increase during Pneumocystis carinii pneumonia in the rat

1996 ◽  
Vol 9 (3) ◽  
pp. 565-570 ◽  
Author(s):  
D.S. Phelps ◽  
T.M. Umstead ◽  
R.M. Rose ◽  
J.A. Fishman
Keyword(s):  
Pneumocystis Carinii ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A
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