APOPTOTIC NEUTROPHILS ARE PHAGOCYTOSED BY FIBROBLASTS WITH PARTICIPATION OF THE FIBROBLAST VITRONECTIN RECEPTOR AND INVOLVEMENT OF A MANNOSE FUCOSE-SPECIFIC LECTIN/

The fate of neutrophils (PMNs) at sites of inflammation is important t o our understanding of many disease processes. Previously, it had been widely assumed that extravasated PMNs inevitably disintegrated before their fragments were removed by local phagocytes, but we have recentl y described an alternative process whereby senescent PMNs undergo apop tosis (programmed cell death). This process leads to macrophage (M phi ) ingestion of the intact cell by a novel phagocytic recognition proce ss. In this study, we show that monolayers of fibroblasts also can sel ectively phagocytose apoptotic PMNs and that the recognition of apopto tic PMNs by fibroblasts involves two distinct mechanisms: one uses the vitronectin receptor, as in M phi ingestion of PMNs; the other uses a mannose/ fucose-specific lectin, which plays no part in M phi phagocy tosis of apoptotic PMNs. The direct interactions between PMNs and fibr oblasts demonstrated herein may have implications for our understandin g of the relationship between inflammation and scarring in many diseas es.