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Inducible cyclooxygenase‐derived 15deoxy Δ 12‐14 PGJ 2 brings about acute inflammatory resolution in rat pleurisy by inducing neutrophil and macrophage apoptosis
Author(s) -
Gilroy Derek W.,
Colville-Nash Paul R.,
McMaster Shaun,
Sawatzky Deborah A.,
Willoughby Derek A.,
Lawrence Toby
Publication year - 2003
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.02-1162fje
Subject(s) - inflammation , macrophage , apoptosis , immunology , medicine , immune system , pleurisy , programmed cell death , granulocyte , biology , in vitro , pleural effusion , biochemistry
Failure of acute inflammation to resolve leads to persistence of the inflammatory response and may contribute to the development of chronic inflammation. Thus, an understanding of inflammatory resolution will provide insight into the etiology of chronic inflammation. In an acute pleurisy, polymorphonuclear leukocytes (PMNs) were found to predominate at the onset of the lesion but decreased in number by undergoing apoptosis, the principal mechanism by which PMNs died in this model. PMNs were progressively replaced by monocytes, which differentiated into macrophages. As with PMNs, macrophages also underwent programmed cell death leading to an abatement of the inflammatory response and eventual resolution. It was found that apoptosis of both these inflammatory cell types was mediated by pro‐resolving cyclooxygenase 2‐derived 15deoxy Δ 12‐14 PGJ 2 , which is uniquely expressed during active resolution. Although PMN programmed cell death is well understood, the observation that macrophages apoptose during resolution of acute inflammation is less well described. These results provide insight into the mechanisms that switch off acute inflammation and prevent complications of wound healing and potentially the development of immune‐mediated chronic inflammation.