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Publisher Summary Inflammation is one of the most complicated processes in the human body, and the promoting and inhibiting mechanisms of inflammation are significant players in the pathogenesis of various pathologic conditions. Basically, inflammation is the body's defense mechanism against endogenous and exogenous noxious stimuli and is controlled by the immune system. Based on its duration, inflammation may be divided into acute and chronic forms. Acute inflammation is usually utilized for elimination of pathologic, tissue-damaging factors and subsides after the elimination of these stimulatory factors. By contrast, in chronic inflammation, the inflammatory process persists, with periodic reactivation and eventual tissue destruction and fibrosis. Inflammation orchestrated by immune system activation plays a crucial role in tissue damage, repair, and remodeling. Persistence of inflammation can induce phenotypical and epigenetic changes in immune cells and fibroblasts. The fibroblasts that originate from mesenchymal stem cells modulate the immune system and stimulate tissue regeneration. When these cells confront persistent inflammation, they induce tissue fibrosis by secreting extraordinary amounts of extracellular matrix. During tissue injury resulting from various underlying pathologies, alterations in cytokine production are observed in the inflamed microenvironment. These cytokines bind to and interact with their specific receptors on different cells and induce aggregation, stimulation, and differentiation of these cells, either locally or systemically. In addition, the produced trophic factors at the site of inflammation facilitates migration of stem cells, particularly mesenchymal stem cells MSCs, and stimulate them to differentiate and secrete specific factors. |
