Experimental acute pancreatitis — a quantification of dynamics at enzymic and histomorphologic levels

Spormann, H; Sokołowski, A.; Letko, G

doi:10.1016/s0344-0338(89)80013-5

Cited by 37 publications

(28 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Fixed tissues were sectioned and then stained with H&E (performed by HistoTec Laboratory). Pancreatitis severity was scored in a blinded fashion as described previously (48).…”

Section: Methodsmentioning

confidence: 99%

Carbon monoxide–based therapy ameliorates acute pancreatitis via TLR4 inhibition

Xue¹,

Habtezion²

2013

J. Clin. Invest.

View full text Add to dashboard Cite

The protective role of hemeoxygenase-1 (HO-1) in various inflammatory conditions is mediated in part by its products, carbon monoxide (CO) and biliverdin. Here we investigated a therapeutic role for CO and COprimed cells in acute pancreatitis (AP). In a mouse model of AP, treatment with CO-releasing molecule-2 (CORM-2) decreased mortality, pancreatic damage, and lung injury. CORM-2 decreased systemic inflammatory cytokines, suppressed systemic and pancreatic macrophage TNF-α secretion, and inhibited macrophage TLR4 receptor complex expression. In both human and mouse cells, CORM-2 inhibited endogenous and exogenous ligand-dependent TLR4 activation, which indicates that CORM-2 could be therapeutic for both early and late stages of AP, which involve sterile-and endotoxin-mediated inflammation, respectively. Mice engrafted with TLR4-deficient hematopoietic cells were protected against caerulein-induced AP. In the absence of leukocyte TLR4 expression, CORM-2 did not confer additional protection, which indicates that CORM-2-dependent effects are mediated via suppression of macrophage TLR4 activation. We determined that CO was directly responsible for the protective effects of CORM-2 in AP, as inactive forms of CORM-2 were ineffective. Importantly, adoptive transfer of CORM-2-primed cells reduced AP. Such a therapeutic approach would translate the beneficial effects of CO-based therapies, avoiding CO-or CO-RM-mediated toxicities in AP and a wide range of diseases.

show abstract

“…Fixed tissues were sectioned and then stained with H&E (performed by HistoTec Laboratory). Pancreatitis severity was scored in a blinded fashion as described previously (48).…”

Section: Methodsmentioning

confidence: 99%

Carbon monoxide–based therapy ameliorates acute pancreatitis via TLR4 inhibition

Xue¹,

Habtezion²

2013

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Histological investigation of the pancreas is a standard procedure in a b c A -control B -caerulein supramaximal C -taurocholate 3.5% experimental acute pancreatitis and gives relevant information about the severity of pancreatic injury [24,33,34]. We adapted the Spormann score for quantification of experimental pancreatic alterations [35] to our model and evaluated pancreatic oedema and necrosis. Supramaximal caerulein caused histological alterations in pancreatic tissue which are mainly characterised by oedema and marginal necrosis.…”

Section: Discussionmentioning

confidence: 99%

Caerulein or taurocholate induced enzymatic and histologic alterations in the isolated perfused rat pancreas

Mantke

Schubert

Röcken

et al. 2008

Langenbecks Arch Surg

View full text Add to dashboard Cite

The isolated perfused rat pancreas is a useful model to investigate pathophysiological mechanisms which are relevant for the early phase of acute pancreatitis. The caerulein and the taurocholate models are transferable to the isolated rat pancreas. Studies on isolated perfused rat pancreas enable pathophysiological investigations of the exocrine pancreas without influence of systemic components, but with preserved morphology.

show abstract

“…This is the first report of acute pancreatitis associated with a complex I deficiency related to a T3231 mutation. In mitochondrial diseases the reduced ATP production in the acinar cells could cause them to be more susceptible to autodigestion and inflammation, as seen after anoxia or ischemia [4]. On the other hand, acute pancreatitis has been recognised as a possible complication of GH therapy with increased enzyme production as a possible mechanism [1].…”

Section: Discussionmentioning

confidence: 99%

Acute pancreatitis after growth hormone treatment: disease or treatment linked?

Beaufort

Beck²,

Seligmann

et al. 2006

Eur J Pediatr

View full text Add to dashboard Cite

Experimental acute pancreatitis — a quantification of dynamics at enzymic and histomorphologic levels

Cited by 37 publications

References 18 publications

Carbon monoxide–based therapy ameliorates acute pancreatitis via TLR4 inhibition

Carbon monoxide–based therapy ameliorates acute pancreatitis via TLR4 inhibition

Caerulein or taurocholate induced enzymatic and histologic alterations in the isolated perfused rat pancreas

Acute pancreatitis after growth hormone treatment: disease or treatment linked?

Contact Info

Product

Resources

About