Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients exhibiting chronic alcohol abuse, the accumulation of fat droplets in pancreatic acinar cells, as well as changes in pancreatic secretion, can be interpreted as early signs of pancreatic damage. Using rats, (the animals were fed for 9 +/- 1 months with a solution of 20% v/v ethanol, combined with either a normal or a fat enhanced diet) we tested whether or not these symptoms are related both to each other and to morphological lesions of the tissue. Based on six separate histological criteria, the lesions were classified into five stages of severity. In order to characterize the secretory capacity of the pancreas, we measured the outputs of lipase, alpha-amylase, trypsin, chymotrypsin, carboxypeptidase A, elastase, and phospholipase A. Compared with the control group, we found that the alcohol-fed animals exhibited a significantly higher degree of morphological damage to the pancreas, as well as an increased frequency of fat accumulation in the acinar cells, and, with the exception of alpha-amylase, a rise in the level of enzyme secretion. In the animals exhibiting the highest degree of tissue damage, however, both fat accumulation and hypersecretion appeared to be diminished. This diminution could possibly be interpreted as the first sign of chronic pancreatitis. Increased consumption of fat did not change either the level of fat accumulation in the acinar cells, or the level of pancreatic secretion. Within the group of alcohol-fed rats, the most pronounced levels of hypersection were found in animals exhibiting cellular fat accumulation. However, the secretion levels of the alcohol-fed animals exhibiting no such fat accumulation did not differ significantly from that of the control group. Therefore, a relationship appears to exist in rats between fat accumulation in acinar cells and the level of pancreatic secretion.
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PMID:[Correlation between acinar cell fat accumulation and secretory capacity of the rat pancreas in the early stage of alcohol-induced pancreatopathy]. 163 69

Chronic pancreatitis (CP) is characterized by mononuclear inflammatory cell infiltration and replacement of the destroyed parenchyma by fibrous tissue. Recently, mast cells have been implicated in chronic inflammatory processes with fibrous tissue deposition. Therefore, the number and distribution of mast cells and their state of activation were evaluated in 12 normal specimens and in 46 specimens of CP with different causes (alcoholic, tropical, and idiopathic). Furthermore, the presence of stem cell factor (SCF), the main mast cell growth factor, and of its receptor, c-kit, was also assessed. In CP tissues, mast cells were localized both in the fibrotic areas and in the residual acinar parenchyma. The total number of mast cells was significantly higher in CP than in the normal pancreas (P < .0001) and correlated positively with the extent of fibrosis and the intensity of inflammation. Immunoglobulin E (IgE)-dependent mast cell activation was higher in CP than in the normal pancreas. No differences in mast cell number or IgE positivity were found among the 3 causes of CP. SCF-and c-kit immunoreactive mast cells were mostly localized in fibrous tissue and around regenerating ducts, which were also positive for c-kit but were negative for SCF. These results suggest that mast cells, activated by an IgE-dependent mechanism and/or by an SCF-c-kit autocrine loop, are a relevant component of the inflammatory infiltrate in CP, independent of the underlying cause. Their localization near degenerating acini and regenerating ducts might indicate that they play a crucial role in tissue destruction and remodeling in CP.
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PMID:Mast cell distribution and activation in chronic pancreatitis. 1172 55

Drug and food allergy in 80% of cases are the cause of duodenal inflammation disrupting the function of the pancreatic ducts. However, in some cases, elimination diet in patients with food allergy does not provide a sufficient effect. The article shows the effect of cross-allergic reactions on recurrent pancreatitis in 28 children with food allergy (mean age 11.7 +/- 2.9 years). As an additional diagnostic criterion the coefficient of degranulation of mast cell in the intestinal mucosa (the ratio of degranulated forms to granulated) was determined, through which the effect of cross-allergic reactions (between food antigens and drugs of animal origin) on the duration and frequency of exacerbations of chronic pancreatitis in children with food sensitization has been shown. The exception of enzyme preparations for children with sensitization to pork and exception of eubiotics prepared using sucrose-gelatin-milk medium for children with sensitization to cow's milk and beef led to feel better in a shorter time (2-3 days) and to reduce the frequency of relapses. Catamnesis observation for 3 years showed that the incidence of recurrent exacerbations of the disease in 11 children with excepted cross-allergic reactions in the first year of follow-up was 9.1%, in the second year--9.1% and in the third year--0%, while in control group (17 children) the frequency of exacerbations was respectively 23.5; 35.3; 35.3%. In patients of the main group there was a slight overall increase of mast cells in the intestinal mucosa from 211.7 to 230.2 mm2 (p > 0.05) with decreasing of degranulated forms from 163.6 to 138.71 mm2 (p > 0.05) and significant increase of granulated forms from 47.41 to 91.51 mm2 (p < 0.05), resulting in a significant decrease in mast cells degranulation coefficient from 3.2 +/- 0.62/mm2 to 1.24 +/- 0.26/mm2 (p < 0.0001). Thus, duodenal etiology of recurrent pancreatitis caused by exposure to food antigens or cross-allergic reactions can be diagnosed with an additional diagnostic criterion--the coefficient of mast cell degranulation, whose exponents greater than 1.5 indicate evidence of antigenic exposure to the mucosa of the duodenum and allergic inflammation.
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PMID:[Can cross-allergic reactions to food antigens be the cause of recurrent pancreatitis in children with food allergies?]. 2505 57