Inflammation is triggered in the innate immune response by
tissue myeloid cells, macrophages in peripheral tissue and microglia in the
nervous system, in response to microbial or endogenous danger signals.
The plasticity of these cells developing into pro-inflammatory
M1 and anti-inflammatory M2 phenotypes is remarkable. Polarization of
macrophages depends on local environmental factors, especially cytokines and
growth factors. Interferon-γ (IFN-γ) and bacterial lipopolysaccharide (LPS) together
polarize macrophage
into the M1 phenotype which produces reactive oxygen species (ROS), nitric
oxide (NO), and inflammatory cytokines such as tumor necrosis factor-α (TNF-α).
However, NO appears to play a negative role in M1 macrophage
differentiation. M2 polarized phenotypes can be polarized by interleukins 4, 10
or 13 (IL-4 or IL-10 or IL-13) and produce anti-inflammatory molecules such as
the autocrine IL-10, and are responsible for tissue remodeling and
angiogenesis.
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