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Apoptotic neutrophils containing Staphylococcus epidermidis stimulate macrophages to release the proinflammatory cytokines tumor necrosis factor-a and interleukin-6
Wilsson, Å., School of Health Sciences, Jönköping University, Jönköping, Sweden.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Medical and Health Sciences, Nursing Science.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Infectious Diseases. Östergötlands Läns Landsting, Centre for Medicine, Department of Infectious Diseases in Östergötland.
Linköping University, Department of Clinical and Experimental Medicine, Infectious Diseases. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Infectious Diseases in Östergötland.
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2008 (English)In: FEMS Immunology and Medical Microbiology, ISSN 0928-8244, E-ISSN 1574-695X, Vol. 53, no 1, 126-135 p.Article in journal (Refereed) Published
Abstract [en]

Staphylococcus epidermidis infections are usually nosocomial and involve colonization of biomaterials. The immune defense system cannot efficiently control the bacteria during these infections, which often results in protracted chronic inflammation, in which a key event is disturbed removal of neutrophils by tissue macrophages. While ingesting uninfected apoptotic neutrophils, macrophages release anti-inflammatory cytokines that lead to resolution of inflammation. In clinical studies, we have previously found elevated levels of the proinflammatory cytokines tumor necrosis factor-alpha (TNF-a) and interleukin-6 in synovial fluid from prostheses infected with coagulase negative staphylococci. We show that macrophages phagocytosing apoptotic neutrophils containing S. epidermidis released TNF-a and interleukin-6, whereas macrophages phagocytosing spontaneously apoptotic neutrophils did not. This difference was not due to dissimilar phagocytic capacities, because macrophages ingested both types of neutrophils to the same extent. The activation was induced mainly by the apoptotic neutrophils themselves, not by the few remaining extracellular bacteria. Macrophages were not activated by apoptotic neutrophils that contained paraformaldehyde-killed S. epidermidis. Proinflammatory reactions induced by clearance of apoptotic neutrophils containing S. epidermidis might represent an important mechanism to combat the infective agent. This activation of macrophages may contribute to the development of chronic inflammation instead of inflammation resolution. © 2008 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved.

Place, publisher, year, edition, pages
2008. Vol. 53, no 1, 126-135 p.
Keyword [en]
Chronic inflammation, Macrophage, Neutrophil, Phagocytosis, Staphylococcus epidermidis infection, TNF-a
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-45989DOI: 10.1111/j.1574-695X.2008.00412.xOAI: oai:DiVA.org:liu-45989DiVA: diva2:266885
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2017-12-13

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Lind, SusanneÖhman, LenaNilsdotter-Augustinsson, Åsa

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Faculty of Health SciencesNursing ScienceInfectious DiseasesDepartment of Infectious Diseases in Östergötland
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