Macrophage/fibroblast coculture induces macrophage inflammatory protein‐1a production mediated by intercellular adhesion molecule‐1 and oxygen radicals
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.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141120/1/jlb0636.pd
