Up-Regulation of TNFα mRNA in the Rat Spleen Following Induction of Acute Pancreatitis

Hughes, Christopher; Henry, James; Kotb, Malak; Lobaschevsky, Andrew; Sabek, Omaima; Gaber, A. Osama

doi:10.1006/jsre.1995.1224

Cited by 28 publications

(10 citation statements)

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“…40 Serum and intrapancreatic concentrations of TNF-α have been shown to be elevated in mice with caerulein induced acute pancreatitis 39. Furthermore, TNF-α mRNA has been shown to be induced in distant organs during the process of bile acid induced acute pancreatitis in rats 41. Serum TNF-α is not however constantly increased in complicated cases of human acute pancreatitis 42.…”

Section: Discussionmentioning

confidence: 99%

A monoclonal anti-interleukin 8 antibody (WS-4) inhibits cytokine response and acute lung injury in experimental severe acute necrotising pancreatitis in rabbits

Osman

Kristensen

Jacobsen

et al. 1998

Gut

111

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Section: Discussionmentioning

confidence: 99%

A monoclonal anti-interleukin 8 antibody (WS-4) inhibits cytokine response and acute lung injury in experimental severe acute necrotising pancreatitis in rabbits

Osman

Kristensen

Jacobsen

et al. 1998

Gut

111

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“…Acinar cells contribute to TNF-production, following activation by the ascitic fluid present in AP [57]. A few hours after the increase in TNF-expression in pancreas, an induction of its mRNA and protein also occurs in lung, liver and spleen [84,86,87].…”

Section: Tnf-and Il-1mentioning

confidence: 99%

Cross-Talk between Oxidative Stress and Pro-Inflammatory Cytokines in Acute Pancreatitis: A Key Role for Protein Phosphatases

Escobar

Pereda²,

Arduini³

et al. 2009

CPD

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Acute pancreatitis is an acute inflammatory process localized in the pancreatic gland that frequently involves peripancreatic tissues. It is still under investigation why an episode of acute pancreatitis remains mild affecting only the pancreas or progresses to a severe form leading to multiple organ failure and death. Proinflammatory cytokines and oxidative stress play a pivotal role in the early pathophysiological events of the disease. Cytokines such as interleukin 1beta and tumor necrosis factor alpha initiate and propagate almost all consequences of the systemic inflammatory response syndrome. On the other hand, depletion of pancreatic glutathione is an early hallmark of acute pancreatitis and reactive oxygen species are also associated with the inflammatory process. Changes in thiol homestasis and redox signaling decisively contribute to amplification of the inflammatory cascade through mitogen activated protein kinase (MAP kinase) pathways. This review focuses on the relationship between oxidative stress, pro-inflammatory cytokines and MAP kinase/protein phosphatase pathways as major modulators of the inflammatory response in acute pancreatitis. Redox sensitive signal transduction mediated by inactivation of protein phosphatases, particularly protein tyrosin phosphatases, is highlighted.

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“…Receptors for TNF‐α are expressed within the pancreas; cultured pancreatic acinar cells produce, release, and respond (by apoptosis) to TNF‐α17. TNF‐α production occurs also at distant sites such as the lung but at a later time point18.…”

Section: Pathophysiology Of Acute Pancreatitismentioning

confidence: 99%

Inflammatory mediators in acute pancreatitis

et al. 2000

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Up-Regulation of TNFα mRNA in the Rat Spleen Following Induction of Acute Pancreatitis

Cited by 28 publications

References 0 publications

A monoclonal anti-interleukin 8 antibody (WS-4) inhibits cytokine response and acute lung injury in experimental severe acute necrotising pancreatitis in rabbits

A monoclonal anti-interleukin 8 antibody (WS-4) inhibits cytokine response and acute lung injury in experimental severe acute necrotising pancreatitis in rabbits

Cross-Talk between Oxidative Stress and Pro-Inflammatory Cytokines in Acute Pancreatitis: A Key Role for Protein Phosphatases

Inflammatory mediators in acute pancreatitis

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