Contribution of Circulating Leukocytes to Cytokine Production in Pancreatic Duct Obstruction-Induced Acute Pancreatitis in Rats

Alterations of Adhesion Molecule Expression and Inflammatory Mediators in Acute Lung Injury Induced by Septic and Non-septic Challenges

“…TNFα and MCP-1 are the early and critical cytokine and chemokine, respectively, in immune responses. It is conflicting whether TNFα levels in the circulation correlate with disease severity or mortality in patients with acute pancreatitis (17,18), although the number of TNFα producing leukocytes in pancreatic tissue was significantly higher than in the circulation (19) and circulating monocytes have been supposed to be responsible for the increase in TNFα during the development of pancreatitis (18). In order to investigate a potential correlation of TNFα levels with pancreatitis-associated lung injury, the present study measured TNFα levels in the circulation, lung tissue and BAL fluid.…”

Study progress on mechanism of severe acute pancreatitis complicated with hepatic injury

“…Many studies show that injury of the over activated neutrocyte on self tissue is an important cause of systemic complications due to AP (Chen et al, 2001;de Dios et al, 2002;Descamps et al, 2003;Ammori, 2003;Shields et al, 2001;Demols and Deviere, 2003;Zhao et al, 2003;Zhou et al, 2002;Song et al, 2002;Brady et al, 2002;Clemons et al, 2002;Hartwig et al, 2002c;Mikami et al, 2002). The neutrophilic granulocyte stimulated by pancreatitis can release inflammatory cytokines such as TNF-α (Cassatella, 1995;Ni et al, 1998;Ogawa, 1998).…”

Pancreatic and bile duct obstruction exacerbates rat caerulein-induced pancreatitis: a new experimental model of acute hemorrhagic pancreatitis

“…de Dios and her colleagues reported that oxygen free radical production in acinar cells and cytokine elevation in plasma were induced by pancreatic duct obstruction in rats and analyzed the time course of these phenomena. 17,18 According to their observations, however, both alterations were induced by 3-h obstruction but not by 1.5-h obstruction, indicating that the involvement of these factors in the present mechanism seems less possible. Moreover, Mooren et al reported 2-h pancreatic duct obstruction in the mouse significantly increased resting intracellular Ca 2+ concentration but depressed CCK-stimulated intracellular Ca 2+ mobilization.…”