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Summaryplays a major role in the pathophysiology of acute pancreatitis (AP). It is an acute inflammatory process of the pancreas, with variable involvement of other regional tissues or remote organ systems. The process of acute inflammation involves cells already present in all tissues, mainly resident macrophages and other cells. Inflammatory mediators believed to participate in the pathophysiology of this condition include: tumor necrosis factor-α, interleukin (IL)-6, IL-1β, IL-10, platelet activating factor, intercellular adhesion molecule-1, IL-8, monocyte chemotactic protein-1, complement component C5a, hydrogen sulfide, neutral endopeptidase and nuclear factor κB. Apart from these mediators, the role of substance P (SP) in the pathogenesis of AP has been described. SP is a neuropeptide that is released from nerve endings in many tissues and acts as a pro-inflammatory mediator in many inflammatory states including AP. This review focuses on the role of macrophages and SP in the pathogenesis of AP. Immunogastroenterology 2012; 1:90-99
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Ramesh Kumar (2012) studied this question.
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