Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The exact immunological mechanisms underlying alcoholic chronic pancreatitis are unclear. To investigate the role of the tumor necrosis factor (TNF) receptor pathway the serum levels of TNF-alpha, soluble TNF receptors -p55/-p75, and CRP were determined by ELISA in 34 patients with late-stage alcoholic chronic pancreatitis and 28 controls. The disease activity (Balthazar scoring system) of acute pancreatitis on the background of late-stage chronic pancreatitis correlated with an increase of functionally active TNF receptor -p55/-p75 serum levels. Unstimulated peripheral blood mononuclear cells are one source of soluble TNF receptors and demonstrated a systemic leukocyte activation. The marked enhancement of soluble TNF receptors suggests that alcoholic chronic pancreatitis may be characterized by transient peaks of in situ TNF-alpha production preceding a long-lasting release of soluble TNF receptors. The data demonstrate immunological changes characteristic of acute pancreatitis in late-stage alcoholic chronic pancreatitis.
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PMID:Immunological changes of mild acute pancreatitis in late-stage alcoholic chronic pancreatitis. 1050 12

Activation of apoptosis in chronic pancreatitis has been demonstrated. The low-affinity neurotrophin receptor p75 (p75NTR) mediates apoptosis in many cell types in vivo and in vitro. The aim of this study was to examine whether p75NTR is involved in the apoptotic process in chronic pancreatitis. The quantity and localization of the receptor was evaluated using northern blot analysis, in situ hybridization, immunohistochemistry, and western blot analysis. Apoptosis was determined by TUNEL assay. By northern blot analysis, p75NTR mRNA levels were increased 40-fold in chronic pancreatitis compared with normal pancreas (P < 0.01). In situ hybridization revealed weak p75NTR mRNA expression in some ductal cells in the normal pancreas. In contrast in chronic pancreatitis moderate p75NTR expression was present in acinar cells next to fibrosis, ductal cells, and cells of ductular structures as well as in some islet cells. Immunostaining of p75NTR in normal pancreas and chronic pancreatitis tissue samples showed a similar intensity and distribution pattern as found by in situ hybridization. Higher p75NTR protein levels could be confirmed by western blot analysis, which revealed an 8.6-fold increase of p75NTR in chronic pancreatitis. TUNEL staining showed, in chronic pancreatitis samples, positivity in some acinar cells next to fibrosis, some ductal cells, and cells of ductular structures. Also some islet cells were positive by TUNEL staining. The presence of p75NTR immunoreactivity was positively correlated (P < 0.05) with the apoptotic index in the exocrine and endocrine pancreas. In conclusion, p75NTR, the low-affinity receptor of neurotrophins which mediates apoptosis, is up-regulated in CP and is involved in the apoptotic process of the exocrine and endocrine pancreas.
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PMID:Up-regulation of p75 neurotrophin receptor (p75NTR) is associated with apoptosis in chronic pancreatitis. 1274 61