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B/Toll-Like Receptor Pathway in Induction of Inflammatory and Tissue-Repair Gene Expression by Necrotic Cells1
* Department of Biological Sciences, Columbia University, New York, NY 10027; and Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520
Tissue damage induced by infection or injury can result in
necrosis, a mode of cell death characterized by induction of an
inflammatory response. In contrast, cells dying by apoptosis do not
induce inflammation. However, the reasons for underlying differences
between these two modes of cell death in inducing inflammation are not
known. Here we show that necrotic cells, but not apoptotic cells,
activate NF-
B and induce expression of genes involved in
inflammatory and tissue-repair responses, including neutrophil-specific
chemokine genes KC and macrophage-inflammatory protein-2, in
viable fibroblasts and macrophages. Intriguingly, NF-B activation by
necrotic cells was dependent on Toll-like receptor 2, a signaling
pathway that induces inflammation in response to microbial agents.
These results have identified a novel mechanism by which cell necrosis,
but not apoptosis, can induce expression of genes involved in
inflammation and tissue-repair responses. Furthermore, these results
also demonstrate that the NF-B/Toll-like receptor 2 pathway can be
activated both by exogenous microbial agents and endogenous
inflammatory stimuli.
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