Published ahead of print on May 4, 2006, doi:10.1165/rcmb.2006-0128OC Am. J. Respir. Cell Mol. Biol., Volume 35, Number 4, October 2006, 474-478 A more recent version of this article appeared on October 1, 2006
Submitted on March 29, 2006 The Macrophage Scavenger Receptor SR-AI/II and Lung Defense against Pneumococci and ParticlesMohamed S Arredouani1,1 Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA, 2 Physiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA; Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA * To whom correspondence should be addressed. E-mail: lkobzik{at}hsph.harvard.edu.
The class A macrophage scavenger receptor SR-AI/II is implicated as a pattern recognition receptor for innate immunity, but its functional role in lung defense has not been studied. We used mice genetically deficient in SR-AI/II and their wild-type C57BL/6 counterparts to investigate the contribution of this receptor to defense against pneumococcal infection and inhaled particles. SR-AI/II deficiency caused impaired phagocytosis of fluorescent bacteria in vivo, diminished clearance of live bacteria from the lungs, and substantially increased pneumonic inflammation. Survival studies also showed increased mortality in SR-AI/II-deficient mice with pneumococcal lung infection. Similarly, after challenge of the airways with TiO2 particles, SR-AI/II-deficient mice showed increased proinflammatory cytokine levels in lung lavage fluid and a more pronounced neutrophilic inflammation. The data indicate that the lung macrophage class A scavenger receptor SRAI/II contributes to innate defense against bacteria and inhaled particles.
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