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(American Journal of Pathology. 2002;161:257-266.)
© 2002 American Society for Investigative Pathology

Regular Articles

Eosinophil Recruitment in Type-2 Hypersensitivity Pulmonary Granulomas

Source and Contribution of Monocyte Chemotactic Protein-3 (CCL7)

Xiao-Zhou Shang*, Bo-Chin Chiu*, Valerie Stolberg{dagger}, Nicholas W. Lukacs*, Steven L. Kunkel*, Hedwig S. Murphy*{dagger} and Stephen W. Chensue*{dagger}

From the Department of Pathology,*University of Michigan Hospitals, Ann Arbor; and the Departments of Pathology and Laboratory Medicine,{dagger}Veterans Affairs Medical Center, Ann Arbor, Michigan

Monocyte chemotactic protein-3 (MCP-3/CCL7) has potent eosinophil chemoattractant properties. The present study determined its relative contribution to the formation of Th2 cytokine-mediated (type-2) eosinophil-rich interstitial lung granulomas induced by antigens of Schistosoma mansoni eggs. Both MCP-3 transcripts and protein levels were more strongly expressed in lungs with type-2 than with type-1 (mycobacterial antigen-elicited Th1-mediated) granulomas. In vivo treatment with neutralizing antibodies demonstrated that MCP-3 abrogated eosinophil accumulation in type-2 lesions by 40 to 50%. Immunohistochemical staining revealed that MCP-3 localized to vessels in or near granulomas suggesting that endothelial cells were an important in situ source of MCP-3. Maximal MCP-3 transcript expression was abrogated by anti-interleukin-4 treatment. Furthermore, cultured mouse lung endothelial cells displayed augmented MCP-3 production in response to interleukin-4. Together, these results suggest that MCP-3 contributes to a significant component of eosinophil recruitment in the type-2 interstitial granuloma formation and Th2 cytokines promote its production.




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