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Am. J. Respir. Crit. Care Med., Volume 164, Number 12, December 2001, 2243-2247

Abnormal Pulmonary Granuloma Formation in Osteopontin-deficient Mice

ANTHONY W. O'REGAN, JASON M. HAYDEN, STEVEN BODY, LUCY LIAW, NIALL MULLIGAN, MARGO GOETSCHKES, and JEFFREY S. BERMAN

Pulmonary Center and Department of Pathology, Boston University School of Medicine, and the Center for Molecular Medicine, Maine Medical Center Research Institute, Boston, Massachusetts

Osteopontin is a novel cytokine that is expressed in pulmonary granulomatous disease such as sarcoidosis and tuberculosis. It can regulate macrophage and T cell migration, activation, and cytokine expression, yet its role in granuloma formation and evolution is unknown. We induced hypersensitivity pulmonary granulomas by embolizing Schistosoma mansoni eggs to the lungs of osteopontin-deficient (null mutant) mice and osteopontin-sufficient (wild-type control) mice. Granulomas from osteopontin-null animals were smaller at early time points and contained remarkably few macrophages and macrophage-derived epithelioid cells and giant cells. T cell accumulation was unaffected by osteopontin deficiency. These results demonstrate that osteopontin regulates macrophage accumulation during pulmonary granuloma formation, and may explain the impaired ability of osteopontin-deficient hosts to control mycobacterial disease.




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