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Macrophage–neutrophil interaction: A paradigm for chronic inflammation revisited
Author(s) -
Lefkowitz Doris L,
Lefkowitz Stanley S
Publication year - 2001
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1046/j.1440-1711.2001.01020.x
Subject(s) - myeloperoxidase , inflammation , immunology , macrophage , tumor necrosis factor alpha , cytokine , downregulation and upregulation , proinflammatory cytokine , medicine , biology , in vitro , biochemistry , gene
Macrophages have been described as ‘factories’ of pro‐inflammatory cytokines. Several years ago the present investigators reported that binding of inactive myeloperoxidase (iMPO) to the macrophage‐mannose receptor resulted in the induction of TNF and other cytokines. Also, if endothelial cells were incubated with iMPO, but not enzymatically active myeloperoxidase (MPO), upregulation of cytokine mRNA and cytokines was observed. Taken in their entirety, the data suggest a dichotomy of function for myeloperoxidase; that is, enzymatically active MPO functions primarily in cell killing through the ‘cytotoxic triad’ and iMPO functions as an immunoregulatory molecule through the induction of numerous cytokines. These studies underscore a previously unrecognized interaction among neutrophils, endothelial cells and macrophages, resulting in the induction of TNF and perpetuation of inflammation . The inflammation induced could be relevant in a number of diseases in which neutrophils play a prominent role. The importance of this interaction in the pathogenesis of rheumatoid arthritis is currently under investigation.