Published ahead of print on May 4, 2006, doi:10.1165/rcmb.2006-0128OC
© 2006 American Thoracic Society DOI: 10.1165/rcmb.2006-0128OC The Macrophage Scavenger Receptor SR-AI/II and Lung Defense against Pneumococci and ParticlesPhysiology Program, Harvard School of Public Health, and Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts Correspondence and requests for reprints should be addressed to Dr. Lester Kobzik, Physiology Program, 665 Huntington Avenue, SPH-II, Room 221, Boston, MA 02115. 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 SR-AI/II contributes to innate defense against bacteria and inhaled particles.
Key Words: environmental particles • lung • macrophages • scavenger receptors This article has been cited by other articles:
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