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Program in Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206
Granulocytes undergoing apoptosis are recognized and removed by
phagocytes before their lysis. The release of their formidable arsenal
of proteases and other toxic intracellular contents into tissues can
create significant damage, prolonging the inflammatory response.
Binding and/or uptake of apoptotic cells by macrophages inhibits
release of proinflammatory cytokines by mechanisms that involve
anti-inflammatory mediators, including TGF-
. To model the direct
effects of necrotic cells on macrophage cytokine production, we added
lysed or apoptotic neutrophils and lymphocytes to mouse and human
macrophages in the absence of serum to avoid complement activation. The
results confirmed the ability of lysed neutrophils, but not
lymphocytes, to significantly stimulate production of
macrophage-inflammatory protein 2 or IL-8, TNF-
, and IL-10.
Concomitantly, induction of TGF-1 by lysed neutrophils was
significantly lower than that observed for apoptotic cells. The
addition of selected serine protease inhibitors and anti-human
elastase Ab markedly reduced the proinflammatory effects, the lysed
neutrophils then behaving as an anti-inflammatory stimulus similar
to intact apoptotic cells. Separation of lysed neutrophils into
membrane and soluble fractions showed that the neutrophil membranes
behaved like apoptotic cells. Thus, the cytokine response seen when
macrophages were exposed to lysed neutrophils was largely due to
liberated proteases. Therefore, we suggest that anti-inflammatory
signals can be given by PtdSer-containing cell membranes, whether from
early apoptotic, late apoptotic, or lysed cells, but can be overcome by
proteases liberated during lysis. Therefore, the outcome of an
inflammatory reaction and the potential immunogenicity of Ags within
the damaged cell will be determined by which signals
predominate.
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B. Endlich, D. Armstrong, J. Brodsky, M. Novotny, and T. A. Hamilton Distinct Temporal Patterns of Macrophage-Inflammatory Protein-2 and KC Chemokine Gene Expression in Surgical Injury J. Immunol., April 1, 2002; 168(7): 3586 - 3594. [Abstract] [Full Text] [PDF]
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A. Byrne and D. J. Reen Lipopolysaccharide Induces Rapid Production of IL-10 by Monocytes in the Presence of Apoptotic Neutrophils J. Immunol., February 15, 2002; 168(4): 1968 - 1977. [Abstract] [Full Text] [PDF]
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S. Somersan, M. Larsson, J. F. Fonteneau, S. Basu, P. Srivastava, and N. Bhardwaj Primary Tumor Tissue Lysates Are Enriched in Heat Shock Proteins and Induce the Maturation of Human Dendritic Cells J. Immunol., November 1, 2001; 167(9): 4844 - 4852. [Abstract] [Full Text] [PDF]
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