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Secondary necrosis of apoptotic neutrophils induced by the human cathelicidin LL-37 is not proinflammatory to phagocytosing macrophages

Journal article
Authors H. N. Li
P. G. Barlow
Johan Bylund
A. Mackellar
Åse Björstad
J. Conlon
P. S. Hiemstra
C. Haslett
M. Gray
A. J. Simpson
A. G. Rossi
D. J. Davidson
Published in J Leukoc Biol
Volume 86
Issue 4
Pages 891-902
ISSN 1938-3673 (Electronic) 1938-3673 (Linking)
Publication year 2009
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages 891-902
Language en
Links www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords Apoptosis/*drug effects, Cathelicidins/*pharmacology, Cell Degranulation/*drug effects, Humans, Macrophages/*metabolism/pathology, Necrosis/metabolism/pathology, Neutrophils/*metabolism/pathology, Phagocytosis/*drug effects
Subject categories Medical and Health Sciences

Abstract

Cathelicidins are CHDP with essential roles in innate host defense but also more recently associated with the pathogenesis of certain chronic diseases. These peptides have microbicidal potential and the capacity to modulate innate immunity and inflammatory processes. PMN are key innate immune effector cells with pivotal roles in defense against infection. The appropriate regulation of PMN function, death, and clearance is critical to innate immunity, and dysregulation is implicated in disease pathogenesis. The efferocytosis of apoptotic PMN, in contrast to necrotic cells, is proposed to promote the resolution of inflammation. We demonstrate that the human cathelicidin LL-37 induced rapid secondary necrosis of apoptotic human PMN and identify an essential minimal region of LL-37 required for this activity. Using these LL-37-induced secondary necrotic PMN, we characterize the consequence for macrophage inflammatory responses. LL-37-induced secondary necrosis did not inhibit PMN ingestion by monocyte-derived macrophages and in contrast to expectation, was not proinflammatory. Furthermore, the anti-inflammatory effects of apoptotic PMN on activated macrophages were retained and even potentiated after LL-37-induced secondary necrosis. However, this process of secondary necrosis did induce the release of potentially harmful PMN granule contents. Thus, we suggest that LL-37 can be a potent inducer of PMN secondary necrosis during inflammation without promoting macrophage inflammation but may mediate host damage through PMN granule content release under chronic or dysregulated conditions.

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