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J Appl Physiol 92: 809-816, 2002; doi:10.1152/japplphysiol.00628.2001
8750-7587/02 $5.00
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Vol. 92, Issue 2, 809-816, February 2002

Pulmonary surfactant and inflammation in septic adult mice: role of surfactant protein A

Jaret L. Malloy1, Ruud A. W. Veldhuizen1, Francis X. McCormack2, Thomas R. Korfhagen3, Jeffery A. Whitsett3, and James F. Lewis1

1 Departments of Physiology and Medicine, Lawson Health Research Institute, University of Western Ontario, London, Ontario, Canada N6A 4V2; 2 Division of Pulmonary and Critical Care, Department of Medicine, University of Cincinnati, Cincinnati, 45267; and 3 Division of Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, Ohio 45229

Surfactant alterations, alveolar cytokine changes, and the role of surfactant protein (SP)-A in septic mice were investigated. Sepsis was induced via cecal ligation and perforation (CLP). Septic and sham mice were euthanized at 0, 3, 6, 9, 12, 15, and 18 h after surgery. Mice deficient in SP-A and mice that overexpressed SP-A were euthanized 18 h after surgery. In wild-type, sham-operated mice, surfactant pool sizes were similar at all time points, whereas in the CLP groups there was a significant decrease in small-aggregate surfactant pool sizes beginning 6 h after CLP. Interleukin-6 concentrations in bronchoalveolar lavage fluid from septic animals increased from 6 to 18 h after surgery. Identical surfactant alterations and concentrations of cytokines were observed in septic mice that were SP-A deficient or that overexpressed SP-A. In conclusion, alterations of pulmonary surfactant and alveolar cytokines occur simultaneously, 6 h after a systemic insult. In addition, we did not detect a role for SP-A in regulating surfactant phospholipid pool sizes or pulmonary inflammation in septic mice.

cecal ligation and perforation; surfactant aggregates; cytokines; in vivo; mouse


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