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  • 1. Lundqvist-Gustafsson, Helen
    et al.
    Norrman, Sara
    Nilsson, J
    Wilsson, Åsa
    Jönköping University, School of Health Science, HHJ, Dep. of Natural Science and Biomedicine.
    Involvement of p38-mitogen-activated protein kinase in Staphylococcus aureus-induced neutrophil apoptosis.2001In: Journal of Leukocyte Biology, ISSN 0741-5400, E-ISSN 1938-3673, Vol. 70, no 4, p. 642-648Article in journal (Refereed)
  • 2. Nilsdotter-Augustinsson, Åsa
    et al.
    Wilsson, Åsa
    Jönköping University, School of Health Science, HHJ, Dep. of Natural Science and Biomedicine.
    Larsson, Jenny
    Stendahl, Olle
    Öhman, Lena
    Lundqvist-Gustafsson, Helen
    Staphylococcus aureus, but not Staphylococcus epidermidis, modulates the oxidative response and induces apoptosis in human neutrophils2004In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 112, no 2, p. 109-118Article in journal (Refereed)
  • 3.
    Wilsson, Åsa
    Jönköping University.
    On the interaction between huamn neutrophils andStaphylococcus aureus2000Doctoral thesis, monograph (Other scientific)
  • 4.
    Wilsson, Åsa
    et al.
    Jönköping University, School of Health and Welfare, HHJ, Dep. of Natural Science and Biomedicine.
    Lind, Sara
    Division of Medical Microbiology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Öhman, Lena
    Division of Medical Microbiology, Linköping University, Linköping, Sweden; and Division of Infectious Diseases, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Nilsdotter-Augustinsson, Åsa
    Division of Infectious Diseases, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Lundqvist-Setterud, Helen
    Division of Medical Microbiology, Linköping University, Linköping, Sweden; Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Apoptotic neutrophils containing Staphylococcus epidermidis stimulate macrophages to release the proinflammatory cytokines tumor necrosis factor-α and interleukin-62008In: FEMS Immunology and Medical Microbiology, ISSN 0928-8244, E-ISSN 1574-695X, Vol. 53, no 1, p. 126-135Article in journal (Refereed)
    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-alpha) 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-alpha 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.

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