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Macrophage/fibroblast coculture induces macrophage inflammatory protein-1α production mediated by intercellular adhesion molecule-1 and oxygen radicals

1998; Oxford University Press; Volume: 64; Issue: 5 Linguagem: Inglês

10.1002/jlb.64.5.636

1938-3673

Matthew L. Steinhauser, Steven L. Kunkel, Cory M. Hogaboam, Holly Evanoff, Robert M. Strieter, Nicholas W. Lukacs,

Immune Response and Inflammation

Abstract This study examined the cell-to-cell interaction between fibroblasts and macrophages as a possible contributor to the chronic inflammatory state. In a coculture system, consisting of macrophages layered over confluent fibroblasts, there was a significant increase in macrophage inflammatory protein 1α (MIP-1α) compared with control cultures. ICAM-1 adhesion was identified as an important stimulus of MIP-1α production by using ICAM-1-specific monoclonal antibodies. Furthermore, fibroblasts from ICAM-1 knockout mice induced significantly less MIP-1α production from peritoneal macrophages when compared to control fibroblasts. In addition, it appeared that oxygen radicals functioned as activating molecules during cellular interaction and production of MIP-1α, as the addition of the antioxidant N-acetylcysteine (NAC) prevented MIP-1α secretion. Thus, the ICAM-1 and oxygen radical-mediated induction of MIP-1α associated with a macrophage/fibroblast coculture system provides one possible mechanism by which immune/inflammatory cell interactions may augment chemokine production and exacerbate chronic inflammatory diseases. J. Leukoc. Biol. 64: 636–641; 1998.