Abstract

Acute pancreatitis is an inflammation that first affects the pancreatic gland but can progress to other organs.Pathophysiological pathways connected to the systemic inflammatory response, with cytokines and oxidative stress as two of their key constituents, mediate the development of severe acute pancreatitis. The primary source of cytokines are activated leukocytes. The majority of the side effects of the systemic inflammatory response syndrome are initiated and spread by interleukin 1ß and tumour necrosis factor alpha (TNF-), which amplifies the inflammatory response. Numerous cell types create cytokines, which are low molecular weight soluble proteins, in response to stress or injury as a way of cell-to-cell communication. The primary source of cytokines, which are consequently crucial elements of the inflammatory cascade, is activated leukocytes. Interleukin 1ß (IL-1ß) and tumour necrosis factor alpha (TNF-) are two of the main members of the cytokine inflammatory family that trigger both the expression of their own cytokines as well as the expression of other cytokines, amplifying the inflammatory response. Nearly all of the effects of the systemic inflammatory response syndrome are started by and spread by these cytokines. Comparatively to those from patients without systemic problems, the monocytes from individuals with acute pancreatitis produce more TNF-, IL-6, and IL-8.