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Departments of 1 Cell Biology and 2 Pediatrics, Duke University, Durham, North Carolina 27710; and 3 Division of Pulmonary Biology, Children's Hospital Research Foundation, Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039
The role
of surfactant-associated protein (SP) A in the mediation of pulmonary
responses to bacterial lipopolysaccharide (LPS) was assessed in vivo
with SP-A gene-targeted [SP-deficient;
SP-A(
/)] and wild-type [SP-A(+/+)]
mice. Concentrations of tumor necrosis factor (TNF)-
, macrophage
inflammatory protein-2, and nitric oxide were determined in recovered
bronchoalveolar lavage fluid after intratracheal administration of LPS.
SP-A(/) mice produced significantly more TNF- and
nitric oxide than SP-A(+/+) mice after LPS treatment. Intratracheal
administration of human SP-A (1 mg/kg) to SP-A(/) mice
restored regulation of TNF-, macrophage inflammatory protein-2, and
nitric oxide production to that of SP-A(+/+) mice. Other markers of
lung injury including bronchoalveolar fluid protein, phospholipid
content, and neutrophil numbers were not influenced by SP-A. Data from
experiments designed to test possible mechanisms of SP-A-mediated
suppression suggest that neither binding of LPS by SP-A nor enhanced
LPS clearance are the primary means of inhibition. Our data and others
suggest that SP-A acts directly on immune cells to suppress LPS-induced
inflammation. These results demonstrate that endogenous or exogenous
SP-A inhibits pulmonary LPS-induced cytokine and nitric oxide
production in vivo.
lipopolysaccharide; lung inflammation
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