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The Journal of Immunology, 2004, 173: 6319-6326.
Copyright © 2004 by The American Association of Immunologists

Pathogen-Induced Apoptotic Neutrophils Express Heat Shock Proteins and Elicit Activation of Human Macrophages1

Limin Zheng2,*,{dagger}, Min He*,{dagger}, Min Long{dagger}, Robert Blomgran{dagger} and Olle Stendahl{dagger}

* Key Laboratory of Gene Engineering of the Education Ministry, Department of Biochemistry, College of Life Sciences, Sun Yatsen (Zhongshan) University, Guangzhou, China; and {dagger} Division of Medical Microbiology, Faculty of Health Sciences, Linkoping University, Linkoping, Sweden

Ingestion of aged or irradiated apoptotic neutrophils actively suppresses stimulation of macrophages (M{phi}). Many bacterial pathogens can also provoke apoptosis in neutrophils, but little is known about how such apoptotic cells influence M{phi} activation. We found that neutrophils undergoing apoptosis induced by UV irradiation, Escherichia coli, or Staphylococcus aureus could either stimulate or inhibit M{phi} activation. In contrast to M{phi} that had ingested irradiated apoptotic neutrophils, M{phi} that had phagocytosed bacteria-induced apoptotic neutrophils exhibited markedly increased production of the proinflammatory cytokine TNF-{alpha}, but not the anti-inflammatory cytokine TGF-{beta}. Moreover, ingestion of bacteria, but not UV-induced apoptotic neutrophils, caused increased expression of Fc{gamma}RI on M{phi}, and this effect was not provoked directly by bacteria associated with the apoptotic neutrophils. Instead, we found that a link between pathogen-induced apoptotic neutrophils and up-regulation of the heat shock proteins HSP60 and HSP70, and we also observed that recombinant HSP60 and HSP70 potentiated LPS-stimulated production of TNF-{alpha} in M{phi}. The opposing macrophage responses to neutrophils undergoing apoptosis induced in different ways may represent a novel mechanism that regulates the extent of the immune response to invading microbes in two steps: first by aiding the functions of M{phi} at an early stage of infection, and subsequently by deactivating those cells through removal of uninfected apoptotic neutrophils. HSP induction in neutrophils may provide the danger signals required to generate a more effective macrophage response.


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