We examined the pancreatic islet lesions in Japanese patients with Type II diabetes mellitus to determine if the damage was related to oxidative stress. Morphometric analyses were performed on immunostained sections of the tail portion of the pancreas from 14 diabetic and 15 non-diabetic patients. Amyloid deposition and oxidative stress-induced tissue damage were evaluated by Congo-red staining and immunostaining. Resistance to oxidative stress was assessed from immunostaining results for Cu, Zn-superoxide dismutase (SOD). Expression of (pro)insulin mRNA was assessed by in situ hybridisation. The pancreas from diabetic patients had amyloid deposition in about 15 % of the islets, intensified reactions of 8-OHdG and HNE, as well as reduced expression of SOD. Islet volume density of beta cells and total beta-cell mass in the pancreas from diabetic patients were reduced by 22 % (p < 0.001) and 30 % (p < 0.05). Islet volume density and total mass of (pro)insulin mRNA-positive cells were similarly reduced in diabetic patients by 22 % (p < 0.001) and 39 % (p < 0.05), respectively. Islet volume density of A cells was increased by 20 % (p < 0.001) but total mass did not change. There were no changes in volume densities of islet, D and PP cells. Reduced beta-cell volume density correlated with increased positive staining of 8-OHdG. Japanese Type II diabetic patients show a reduction of beta-cell mass and evidence of increased oxidative stress-related tissue damage that is correlated with the extent of the beta-cell lesions. [Diabetologia (2002) 45: 85–96]

/pdf/reduced-beta-cell-mass-and-expression-of-oxidative-stress-192atn264m.pdf

Reduced beta-cell mass and expression of oxidative stress-related DNA damage in the islet of Japanese Type II diabetic patients.

Obstacles Posed by the Tumor Microenvironment to T cell Activity: A Case for Synergistic Therapies

Background: It is now generally accepted that chronic pancreatic injury and fibrosis may result from repeated episodes of acute pancreatic necroinflammation (the necrosis-fibrosis sequence). Recent studies suggest that pancreatic stellate cells (PSCs), when activated, may play an important role in the development of pancreatic fibrosis. Factors that may influence PSC activation during pancreatic necroinflammation include cytokines known to be important in the pathogenesis of acute pancreatitis, such as tumour necrosis factor α (TNF-α), and the interleukins 1, 6, and 10 (IL-1, IL-6, and IL-10).

Aim: To determine the effects of these cytokines on PSC activation, as assessed by cell proliferation, α smooth muscle actin (α-SMA) expression, and collagen synthesis.

Methods: Cultured rat PSCs were incubated with cytokines for 24 hours. Cell proliferation was assessed by measuring 3H thymidine incorporation into cellular DNA, α-SMA expression by western blotting, and collagen synthesis by incorporation of 14C proline into collagenase sensitive protein. mRNA levels for procollagen α1(1) in PSCs were determined by northern and dot blotting methods.

Results: Expression of α-SMA by PSCs was increased on exposure to each of the cytokines used in the study. Stellate cell proliferation was stimulated by TNF-α but inhibited by IL-6, while IL-1 and IL-10 had no effect on PSC proliferation. Collagen synthesis by PSCs was stimulated by TNF-α and IL-10, inhibited in response to IL-6, and unaltered by IL-1. Changes in collagen protein synthesis in response to TNF-α, IL-10, and IL-6 were not regulated at the mRNA level in the cells.

Conclusion: This study has demonstrated that PSCs have the capacity to respond to cytokines known to be upregulated during acute pancreatitis. Persistent activation of PSCs by cytokines during acute pancreatitis may be a factor involved in the progression from acute pancreatitis to chronic pancreatic injury and fibrosis.

https://gut.bmj.com/content/gutjnl/50/4/535.full.pdf

Pancreatic stellate cells respond to inflammatory cytokines: potential role in chronic pancreatitis

While the morphology and function of cells of the exocrine and endocrine pancreas have been studied over several centuries, one important cell type in the gland, the pancreatic stellate cell (PSC), had remained undiscovered until as recently as twenty years ago. Even after its first description in 1982, it was to be another 16 years before its biology could begin to be studied, because it was only in 1998 that methods were developed to isolate and culture PSCs from rodent and human pancreas. PSCs are now known to play a critical role in pancreatic fibrosis, a consistent histological feature of two major diseases of the pancreas - chronic pancreatitis and pancreatic cancer. In health, PSCs maintain normal tissue architecture via regulation of the synthesis and degradation of extracellular matrix (ECM) proteins. Recent studies have also implied other additional functions for PSCs as progenitor cells, immune cells or intermediaries in exocrine pancreatic secretion in humans. During pancreatic injury, PSCs transform from their quiescent phase into an activated, myofibroblast-like phenotype that secretes excessive amounts of ECM proteins leading to the fibrosis of chronic pancreatitis and pancreatic cancer. An ever increasing number of factors that stimulate and/or inhibit PSC activation via paracrine and autocrine pathways are being identified and characterized. It is also now established that PSCs interact closely with pancreatic cancer cells to facilitate cancer progression. Based on these findings, several therapeutic strategies have been examined in experimental models of chronic pancreatitis as well as pancreatic cancer, in a bid to inhibit/retard PSC activation and thereby alleviate chronic pancreatitis or reduce tumour growth in pancreatic cancer. The challenge that remains is to translate these pre-clinical developments into clinically applicable treatments for patients with chronic pancreatitis and pancreatic cancer.

/pdf/pancreatic-stellate-cells-a-starring-role-in-normal-and-pac8rjgrr9.pdf

Pancreatic stellate cells: a starring role in normal and diseased pancreas

https://www.gastrojournal.org/article/S0016-5085(13)00197-2/pdf

Role of Immune Cells and Immune-Based Therapies in Pancreatitis and Pancreatic Ductal Adenocarcinoma

Background/Aims: Chronic pancreatitis is histologically characterized by an extended fibrosis and infiltration of leukocytes. We intended to differentiate the infiltration to evalua

Immunohistochemical Characterization of the Pancreatic Cellular Infiltrate in Normal Pancreas, Chronic Pancreatitis and Pancreatic Carcinoma

Conclusion
Cu/Zn-SOD is present in pancreatic juice and tissue. Immunohistochemical studies reveal a localization of this enzyme in islet, duct, and centroacinar cells, but to a much lower extent in pancreatic acinar cells.

Cu/Zn-SOD in human pancreatic tissue and pancreatic juice.

Activation of pancreatic stellate cells in experimental chronic pancreatitis in rats

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Immunohistochemical Characterization of the Pancreatic Cellular Infiltrate in Normal Pancreas, Chronic Pancreatitis and Pancreatic Carcinoma

Cu/Zn-SOD in human pancreatic tissue and pancreatic juice.

Activation of pancreatic stellate cells in experimental chronic pancreatitis in rats