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Department of Surgery, Division of Surgical Research, Rhode Island Hospital, and Program in Pathobiology, Brown University School of Medicine, Providence, RI 02903
Macrophages (M
) contribute to the resolution of early
inflammation by recognizing and ingesting apoptotic polymorphonuclear
neutrophils (PMN). In addition, experiments reported here demonstrated
that M can actively induce PMN apoptosis. Coculture of cells from 2-
or 5-day-old wounds in rats, or of M purified from such
preparations, with PMN-rich wound cell populations obtained 1 day after
wounding increased PMN apoptosis by >3-fold. Neither resident- nor
Proprionibacterium acnes-elicited peritoneal
M-induced PMN apoptosis. Apoptosis was not mediated by a soluble
factor and required E:T contact. Fixed wound-M and membrane isolates
from viable M were as effective as intact cells in inducing PMN
apoptosis. M-induced apoptosis was inhibited by peptide
Arg-Gly-Asp-Ser, anti-ß3 (CD61) Ab, CD36 peptide, or
anti-TNF-
Ab. Soluble TNF- did not induce PMN apoptosis. In
additional studies, K562 cells (negative for ß3, TNF-,
and Fas ligand) transfected to express either
vß3 integrin, an uncleavable membrane form
of TNF-, or both were used in cocultures with wound PMN. Only the
double transfectants were able to induce PMN apoptosis, an effect
inhibited by anti-ß3 (CD61) or anti-TNF- Abs.
These results demonstrate that wound M induce PMN apoptosis through
a constitutive effector mechanism requiring both intercellular binding
through integrin-ligand interactions and membrane-bound
TNF-.
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