Surfactants are detergent-like substances in the lungs that dramatically lower the surface tension of the fluid within the air sacs. Particles—including infectious microbes—locate to the distal airspaces during each breath, but the role of surfactants in rapid bacterial clearance in the alveoli has been unclear. In the May 15 Journal of Clinical Investigation, Huixing Wu and colleagues at the University of Cincinnati show that surfactant associated proteins A and D (SP-A, SP-D—also known as collectins) inhibit the growth of Gram-negative bacteria by increasing membrane permeability (Journal of Clinical Investigation, 111:1589-1602, May 15, 2003).

Wu et al. generated SP-A–null mice and SP-D–overexpressing mice and exposed them to Escherichia coli K12. They observed that bacterial pulmonary clearance was reduced in SP-A–null mice and was increased in SP-D–overexpressing mice, compared with strain-matched wild-type controls. In addition, they showed that purified SP-A and SP-D inhibited bacterial synthetic functions of several, but not all, strains of E. coli, Klebsiella pneumoniae, and Enterobacter aerogenes by increasing membrane permeability through a C-terminal domain-dependent mechanism.

"Cooperative interactions of SP-A and SP-D with other antimicrobial proteins in the epithelial lining fluid may result in synergistic inhibition of bacterial proliferation. The reduced collectin levels found in the BAL fluid in idiopathic pulmonary fibrosis, Gram-negative pneumonia, and cystic fibrosis may play a role in the pathogenesis of acute or recurrent infections in those diseases," conclude the authors.