Mast Cells Contribute to Early Pancreatitis-Induced Systemic Endothelial Barrier Dysfunction

Dib, Marwan; Zhao, Xia; Wang, Xiangdong; Andersson, Roland

doi:10.1159/000065087

Cited by 17 publications

(7 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Szabo et al [31] reported that 30 min segmental ischemia and 120 min reperfusion induced significant tissue injury, elevated the segmental vascular resistance, and decreased intramucosal pH (pHi), and CS pretreatments prior to ischemia significantly inhibited the permeability changes, but did not influence the pHi and morphological alterations induced by ischemia-reperfusion, they conclude that intestinal mast cells and mast cell-induced reactions contribute to the mucosal permeability alterations during reperfusion, but play only a minor role in ischemia-reperfusion-induced structural injury. Pretreatment with CS protecting against degranulation, caused a significant impairment of plasma exudation at 30 min of inflammation corresponding to a significantly decreased level of histamine, one of the most potent vasoactive factors released from activated mast cells [32] . The results in our study showed that the injury of small intestinal villus and microvillus was alleviated after CS pretreatment prior to reperfusion and that the ultrastructure of IMMC was basically normal.…”

Section: Discussionmentioning

confidence: 99%

Pretreatment of cromolyn sodium prior to reperfusion attenuates early reperfusion injury after the small intestine ischemia in rats

Hei¹

2007

WJG

View full text Add to dashboard Cite

AIM:To investigate the effects of Cromolyn Sodium (CS) pretreated prior to reperfusion on the activity of intestinal mucosal mast cells (IMMC) and mucous membrane of the small intestine in ischemia-reperfusion (IR) injury of rats. METHODS:Thirty-two Sprague-Dawley (SD) rats were randomly divided into four groups: sham group (group S), model group (group M), high and low dosage of CS groups, (treated with CS 50 mg/kg or 25 mg/kg, group C1 and C2). Intestinal IR damage was induced by clamping the superior mesenteric artery for 45 min followed by reperfusion for 60 min. CS was intravenouly administrated 15 min before reperfusion. Ultrastructure and counts of IMMC, intestinal structure, the expression of tryptase, levels of malondisldehyde (MDA), TNF-α, histamine and superoxide dismutase (SOD) activity of the small intestine were detected at the end of experiment. RESULTS:The degranulation of IMMC was seen in group M and was attenuated by CS treatment. Chiu's score of group M was higher than the other groups. CS could attenuate the up-regulation of the Chiu's score, the levels of MDA, TNF-α, and expression of tryptase and the down-regulation of SOD activity and histamine concentration. The Chiu's score and MDA content were negatively correlated, while SOD activity was positively correlated to the histamine concentration respectively in the IR groups. CONCLUSION:Pretreated of CS prior to reperfusion protects the small intestine mucous from ischemiareperfusion damage, the mechanism is inhibited IMMC from degranulation.

show abstract

Section: Discussionmentioning

confidence: 99%

Pretreatment of cromolyn sodium prior to reperfusion attenuates early reperfusion injury after the small intestine ischemia in rats

Hei¹

2007

WJG

View full text Add to dashboard Cite

show abstract

“…Thereafter, the model was employed frequently to explore the pathogenesis of AP with a commonly adopted regimen of 200 µl of 5% Na‐TDC in the rat. Common findings included the perturbation of energy metabolism in the intestinal wall, 44 impaired intestinal permeability, 45 bacterial translocation, 46,47 formation of platelet‐activating factor, 48 pulmonary endothelial barrier dysfunction, 49 microvascular endothelial barrier dysfunction, 50 activation of mast cells, 51–53 induction of nitric oxide synthase, 54 over‐induced polyamine catabolism, 55–57 increased high‐mobility group box, 58 increased catalytic activity of phospholipase A, 59 upgraded cytokine levels 60,61 and increased myeloperoxidase (MPO) activity 61 …”

Section: Induction Of Ap By Bile Saltsmentioning

confidence: 99%

Review of experimental animal models of biliary acute pancreatitis and recent advances in basic research

Wan

Huang

Latawiec

et al. 2012

HPB

View full text Add to dashboard Cite

Acute pancreatitis (AP) is a formidable disease, which, in severe forms, causes significant mortality. Biliary AP, or gallstone obstruction-associated AP, accounts for 30-50% of all clinical cases of AP. In biliary AP, pancreatic acinar cell (PAC) death (the initiating event in the disease) is believed to occur as acinar cells make contact with bile salts when bile refluxes into the pancreatic duct. Recent advances have unveiled an important receptor responsible for the major function of bile acids on acinar cells, namely, the cell surface G-protein-coupled bile acid receptor-1 (Gpbar1), located in the apical pole of the PAC. High concentrations of bile acids induce cytosolic Ca(2+) overload and inhibit mitochondrial adenosine triphosphate (ATP) production, resulting in cell injury to both PACs and pancreatic ductal epithelial cells. Various bile salts are employed to induce experimental AP, most commonly sodium taurocholate. Recent characterization of taurolithocholic acid 3-sulphate on PACs has led researchers to focus on this bile salt because of its potency in causing acinar cell injury at relatively low, sub-detergent concentrations, which strongly implicates action via the receptor Gpbar1. Improved surgical techniques have enabled the infusion of bile salts into the pancreatic duct to induce experimental biliary AP in mice, which allows the use of these transgenic animals as powerful tools. This review summarizes recent findings using transgenic mice in experimental biliary AP.

show abstract

“…MCs expressing the vesicular monoamine transporter 2 (VAMT2), responsible of the storage and release of polyamines, have been identified in the pancreas of humans and rodents . Consistently, activation and degranulation of MCs generally contribute to the initiation and progression of the disease in different models of acute and chronic pancreatitis, in rat and mice …”

Section: Pancreatic Mast Cellsmentioning

confidence: 94%

Is it time for a new classification of mast cells? What do we know about mast cell heterogeneity?

Frossi

Mion

Sibilano

et al. 2018

Immunological Reviews

View full text Add to dashboard Cite

Mast cells (MCs) are derived from committed precursors that leave the hematopoietic tissue, migrate in the blood, and colonize peripheral tissues where they terminally differentiate under microenvironment stimuli. They are distributed in almost all vascularized tissues where they act both as immune effectors and housekeeping cells, contributing to tissue homeostasis. Historically, MCs were classified into 2 subtypes, according to tryptic enzymes expression. However, MCs display a striking heterogeneity that reflects a complex interplay between different microenvironmental signals delivered by various tissues, and a differentiation program that decides their identity. Moreover, tissue-specific MCs show a trained memory, which contributes to shape their function in a specific microenvironment. In this review, we summarize the current state of our understanding of MC heterogeneity that reflects their different tissue experiences. We describe the discovery of unique cell molecules that can be used to distinguish specific MC subsets in vivo, and discuss how the improved ability to recognize these subsets provided new insights into the biology of MCs. These recent advances will be helpful for the understanding of the specific role of individual MC subsets in the control of tissue homeostasis, and in the regulation of pathological conditions such as infection, autoimmunity, and cancer.

show abstract

Mast Cells Contribute to Early Pancreatitis-Induced Systemic Endothelial Barrier Dysfunction

Cited by 17 publications

References 27 publications

Pretreatment of cromolyn sodium prior to reperfusion attenuates early reperfusion injury after the small intestine ischemia in rats

Pretreatment of cromolyn sodium prior to reperfusion attenuates early reperfusion injury after the small intestine ischemia in rats

Review of experimental animal models of biliary acute pancreatitis and recent advances in basic research

Is it time for a new classification of mast cells? What do we know about mast cell heterogeneity?

Contact Info

Product

Resources

About