title: Proinflammatory stimuli enhance phagocytosis of apoptotic cells by neutrophil granulocytes.
abstract: Recently, we have reported that, in addition to macrophages, also neutrophil granulocytes can phagocytose apoptotic neutrophils. Based on this finding, we hypothesized that "cannibalistic" neutrophils at sites of acute infection/inflammation play a major role in the clearance of apoptotic neutrophils. Since at sites of infection/inflammation neutrophils are exposed to microbial constituents and proinflammatory cytokines, in the present study we analyzed the effect of TLR-ligands and cytokines on the ability of neutrophils to phagocytose apoptotic cells in vitro. We observed that exposure to ligands of TLR2 (Malp2, Pam3CSK4), TLR4 (LPS), TLR7/TLR8 (R848), and TLR9 (ODN 2006) led to increased phagocytosis of apoptotic cells by neutrophils. In addition, proinflammatory cytokines such as TNF and GM-CSF strongly enhanced the uptake of apoptotic cells by neutrophils. These results support the hypothesis that neutrophils acquire the ability to phagocytose apoptotic cells at sites of acute infection/inflammation and thereby can contribute to the resolution of inflammation.
authors: Institute for Medical Microbiology and Hygiene, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany.
authors: Lars
authors: L
authors: Hellberg
authors: Sabrina
authors: S
authors: Fuchs
authors: Christoph
authors: C
authors: Gericke
authors: Arup
authors: A
authors: Sarkar
authors: Martina
authors: M
authors: Behnen
authors: Werner
authors: W
authors: Solbach
authors: Tamás
authors: T
authors: Laskay
mesh_terms: D000328:Adult; D017209:Apoptosis; D006098:Granulocytes / Q000166:cytology*; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology*; D009504:Neutrophils / Q000166:cytology*; D010587:Phagocytosis
chemical_list: D018836:Inflammation Mediators