Tissue-specific cytokine production during experimental acute pancreatitis : A probable mechanism for distant organ dysfunction

摘要: Our purpose was to determine if cytokines are produced systemically during acute pancreatitis. Proinflammatory elevated pancreatitis and have been implicated in the progression of pancreatitis-associated multiple organ dysfunction. Whether these mediators within all tissues or very few specific organs is not known. Edematous induced adult male mice by IP injection cerulein. Necrotizing young female feeding a choline-deficient, ethionine supplemented diet.Animals were sacrificed as worsened, with prepared for tissue mRNA protein analysis RT-PCR immunoblotting.Pancreatitis severity established histologic grading serum amylase lipase. There no cytokine detectable prior induction Tumor necrosis factor-α (TNF-α) interleukin-1-β (IL-1β) detected pancreas early course both models,coinciding development hyperamylasemia (both P < 0.001). Interleukin-6 after more fully developed (P< IL-1β TNF-α subsequently large amounts lung, liver, spleen but never kidney, cardiac muscle, skeletal muscle.A significant delay between pancreatic distant production always observed.It concluded that proinflammatory known develop dysfunction severe Cytokine specific,correlates disease severity, occurs first organs.