Immune function early in acute pancreatitis

Widdison, Adam L.; Cunningham, Steve

doi:10.1002/bjs.1800830514

Cited by 44 publications

(27 citation statements)

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“…CD8+ cells are known as cytotoxic T lymphocytes and some of them differentiate into T8 suppressor cells. A significant depletion of peripheral blood CD4+ and CD8+ subsets of T lymphocytes in the course of AP has been previously reported by others [15][16][17][18][19][20] . However, observations made by the others were mostly restricted to one or up to three different time periods of pancreatitis.…”

Section: Discussionmentioning

confidence: 79%

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Monocyte Subsets and Natural Killer Cells in Acute Pancreatitis

et al. 2008

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Section: Discussionmentioning

confidence: 79%

“…In a small number of studies, disorders in lymphocyte subsets and their function in early S-AP have been reported [15][16][17][18][19][20] . Natural killer cells (NK cells) are a group of cytolytic lymphocytes, distinct from B lymphocytes and T lymphocytes, that participate in both innate immunity and adaptive immunity.…”

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confidence: 99%

Monocyte Subsets and Natural Killer Cells in Acute Pancreatitis

et al. 2008

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“…1,2 Immunologic impairment in the early phase may be linked to the increased susceptibility to subsequent infection and the development of septic complications. Several investigators have reported a reduction of the peripheral lymphocyte count in acute pancreatitis, [3][4][5][6][7] which may indicate immunologic impairment. Curley et al 4 reported a significant decrease in the proportion of CD4-positive lymphocytes (T-helper cells) in SAP.…”

Section: Introductionmentioning

confidence: 97%

Immunosuppression in patients with severe acute pancreatitis

et al. 2006

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“…These cytokines are known to activate neutrophil granulocytes that develop metabolic hyperactivity in severe acute pancreatitis. 37 Elevated cytokine levels and granulocyte hyperactivation are associated with impaired function of the phagocytic cells, 38,39 again resulting in an inadequate clearance of endotoxin and harmful protease-antiprotease complexes.…”

Section: Discussionmentioning

confidence: 99%

Reticuloendothelial System Blockade Promotes Progression from Mild to Severe Acute Pancreatitis in the Opossum

Schleicher¹,

Baas²,

Elser³

et al. 2001

Annals of Surgery

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ObjectiveTo examine the relation between hepatic reticuloendothelial system (RES) dysfunction and the development of acute biliary pancreatitis. In an opossum model, the authors tested the hypothesis that RES blockade can turn the mild pancreatitis seen after pancreatic duct obstruction (PDO) into the severe form. Summary Background DataBiliary obstruction is considered the decisive event in gallstone pancreatitis. Suppression of the RES occurs during biliary obstruction. MethodsEighteen opossums were placed into three groups of six animals each: group A, RES blockade with -carrageenan; group B, PDO; and group C, PDO and RES blockade with carrageenan. The severity of pancreatitis was evaluated by enzyme serum levels and percentage of pancreatic tissue necrosis. RES capacity was measured by dynamic liver scintigraphy, and hepatic blood flow was documented using the hydrogen clearance technique. ResultsNo changes in hepatic blood flow occurred in groups A to C. RES capacity was suppressed in groups A and C; in group B, RES function remained unchanged. In group A, amylase and lipase levels remained normal, 3 Ϯ 1.9% of pancreatic tissue were necrotic. The animals in group B developed mild edematous pancreatitis with an increase in amylase and lipase levels and 15 Ϯ 10% of pancreatic necrosis. In group C, amylase and lipase increased significantly and histology revealed severe necrotizing pancreatitis, with 72 Ϯ 11% of necrotic areas. ConclusionsArtificial RES blockade can promote the progression from mild pancreatitis as observed after PDO to the severe necrotizing form of the disease. Thus, RES dysfunction resulting from biliary obstruction might be an important cofactor in the pathogenesis of bile-induced pancreatitis.Acute biliary pancreatitis is an inflammatory disease that varies in severity and outcome. Mild edematous pancreatitis usually results in morphologic and functional recovery, whereas severe necrotizing pancreatitis is often associated with multisystemic complications and a death rate of 10% to 50%. 1 The reason for this variety in manifestation is not known. The identification of factors determining the severity of acute pancreatitis is essential to improve the understanding of the pathophysiology of bile-induced pancreatitis and its complications.Obstruction of the terminal biliopancreatic ductal system is considered to be the triggering event in human gallstone pancreatitis. Opie, 2 in 1901, postulated that reflux of bile, caused by a gallstone impacted in a common terminal biliopancreatic duct, initiates the process of pancreatic inflammation. Today, most authors disagree with this socalled common channel theory, and not reflux of bile but simultaneous obstruction of the biliary and the pancreatic ducts and their pathophysiologic consequences are considered to be the determining factors in the development of severe pancreatitis.

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Immune function early in acute pancreatitis

Cited by 44 publications

References 44 publications

Monocyte Subsets and Natural Killer Cells in Acute Pancreatitis

Monocyte Subsets and Natural Killer Cells in Acute Pancreatitis

Immunosuppression in patients with severe acute pancreatitis

Reticuloendothelial System Blockade Promotes Progression from Mild to Severe Acute Pancreatitis in the Opossum

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