The sequence of chronic inflammation centres around the activity of macrophages derived from blood monocytes. Most frequently, due to slower migration than neutrophils, they arrive at the site of inflammation after around 48 hours. In certain infections e.g. viral, they are the first cells to arrive.
The stimulus for transit is chemotactic factors released by the inflammatory agent or cells already at the scene e.g. lymphokines, PDGF, TFG beta, complement component C5a. The same range of substances ensure that during transit, macrophages are activated: primed for phagocytosis and intracellular killing.
Once at the site of inflammation, the macrophage is incapable of completing its role. This may be because:
As a consequence, more monocytes are recruited from the blood, more macrophages proliferate locally, and both groups are effectively stranded at the site. Increased macrophage activity and local destruction liberates a number of cytokines including interleukins and growth factors. These attract a range of supplementary cells including lymphocytes, fibroblasts, plasma cells, eosinophils and mast cells. The interaction between various cells is essential: lymphocytes and macrophages act in a complementary manner, each inducing the other's proliferation and differentiation via mediators such as interferon and interleukins.
Growth factors released in a haphazard manner cause random matrix-deposition, angiogenesis and epithelialization.
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