Apoptotic neutrophils activates the inflammatory response in macrophages –increased capacity to handle intracellular infection
(English)Manuscript (preprint) (Other (popular science, discussion, etc.))
Inflammation is essential to eradicate invading pathogens but an uncontrolled inflammation may develop into chronic inflammation and extensive tissue destruction unable of effectively controlling infections. At the site of infection, macrophages are the major regulators of the inflammatory response through balanced release of pro- or anti-inflammatory cytokines and therefore a key cell in the resolution of inflammation. Neutrophils effectively phagocytose and kill pathogens but they are short-lived and removal of these dead cells by macrophages is a key event in the resolution of inflammation and tissue repair.
However, down-regulation of the immune response by apoptotic cells would in the presence of pathogens be detrimental to the host. In contrast to resolution of inflammation, we show that in the presence of microbial stimuli, apoptotic neutrophils in fact exert a potent pro-inflammatory activation of macrophages. This augmentation of the pro-inflammatory response is dependent on uptake of the apoptotic cells by the macrophage. In addition to secretion of TNF-α, presence of apoptotic neutrophils enhanced the capacity of the stimulated macrophages to kill intracellular Mycobacterium tuberculosis. This presents a novel role for apoptotic neutrophils in the modulation of the macrophage-dependent inflammatory response, and control of intracellular infections.
Microbiology in the medical area
IdentifiersURN: urn:nbn:se:liu:diva-20837OAI: oai:DiVA.org:liu-20837DiVA: diva2:236462