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)

Nicotine 5, 25 or 50 micrograms/ml drinking water given ad lib for 5, 10 or 20 days, dose- and time-dependently worsened cold-restraint-induced (stress) ulceration in rat stomachs. Treatment with nicotine 5 or 25 micrograms/ml did not influence the number of gastric mucosal mast cells degranulated by cold and restraint; however, drinking 50 micrograms/ml for 10 days lowered further the mast cell count in stressed animals. During 20-day nicotine administration, the daily food intake and body weight gain, up to the 18th day when the animals were starved before experiments, were not affected by the three concentrations of the alkaloid, except that fluid consumption tended to be less only in those animals given the highest dose. The findings indicate that chronic nicotine treatment exacerbates the severity of stress-evoked ulcer formation. The ulcer-intensifying mechanism of the two lower doses of nicotine appears not to be related to additional mast cell degranulation; only the ulcerogenic action of the highest concentration includes this factor. It is unlikely that ulcer aggravation by nicotine is due to malnutrition because body weight gain and solid food intake by the alkaloid-treated rats were normal.
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PMID:Chronic nicotine treatment intensifies gastric ulceration by cold-restraint stress in rats. 195 Aug 22

To examine the effects of protein malnutrition on mast cells, rats were fed a protein-deficient diet (0.5% protein ad libitum) or normal diet (27% protein ad libitum or pair fed) for 16, 21, 27, or 57 d. Male rats in the different groups showed no significant differences in mast cell number or histamine content per mast cell. IgE binding sites as measured by flow cytometry were decreased in rats on the deficient diet. Even after stripping receptors of endogenous IgE and then labeling with fluorescent IgE, the difference remained, thus confirming the lower number of mast cell IgE receptors in rats maintained on the protein-deficient diet.
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PMID:Protein malnutrition: effect on rat peritoneal mast cell number, histamine content, and IgE receptors. 252 33

Thirteen patients with systemic mast cell disease were studied in order to define the hepatic changes in this disease and to correlate the histologic lesions in the liver with the clinical findings. These patients often presented with multisystem disorders and 10 had hepatomegaly. Microscopically, the liver tissues in all patients showed fibrosis and chronic inflammatory cellular infiltration with plasma cells, lymphocytes, eosinophils, and mononuclear fibroblast-like cells in the portal area. The hepatic sinusoids were not significantly involved. A histologic diagnosis of systemic mast cell disease is seldom entertained in liver biopsy specimens embedded in paraffin and stained with hematoxylineosin, but can be facilitated in biopsy specimens embedded in plastic such as methacrylate. Tissue mast cells in the cellular infiltrate can be demonstrated best by special staining techniques with Giemsa, toluidine blue, and chloroacetate esterase. The severity of the histologic changes in the liver does not correlate well with the size of the liver or biochemical changes in the blood. Abnormal serum biochemical values were noted primarily in those with dehydration caused by diarrhea and vomiting, and in those with malnutrition. Hepatic function test results were usually normal, except for alkaline phosphatase level, which was elevated in all 13 patients. Although the clinical significance of hepatic involvement in systemic mast cell disease cannot be established with certainty in this study, it is believed that the prognosis of systemic mast cell disease is most intricately related to the systemic effects of mast cell involvement in many other organs, and not to hepatic involvement per se.
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PMID:Hepatic involvement in systemic mast cell disease. 370 70

Coeliac disease is a malabsorptive disorder caused by intolerance to gluten and is characterized by a remodelling of the intestinal mucosa including villus atrophy, crypt hyperplasia and net increase of mucosal volume. Changes of the number of mucosal mast cells (MMCs) in coeliac mucosa has recently been reported, suggesting that the mast cell activity could have a pathogenetic role in gluten enteropathy. MMCs located solely in the lamina propria are the main repository for small-gut mucosal histamine. A consecutive prospective study was designed to study the histamine content, MMC numbers, and the relative volume of lamina propria in intestinal biopsies from adult patients suffering from unexplained diarrhea and/or malnutrition. Histamine was measured by a HPLC-method, the number of MMC was counted after long toluidine-blue staining, and the relative volumes of lamina propria and epithelium were estimated morphometrically. The findings were correlated to the histopathological appearance of the mucosa. As compared to controls the histamine content increased by 80% and MMC numbers by about 60% in the coeliac mucosa. There was also a correlation between MMC numbers and histamine content for both normal and coeliac mucosae (r = 0.81). The morphometric estimation of the relative volumes of epithelium and lamina propria revealed that the lamina-propria compartment was increased by approximately 40% in coeliac mucosa. Taking the changes in compartmental volumes of the remodelled coeliac mucosa into account, our results suggest that the histamine content and MMC population were significantly increased. MMC and MMC-associated histamine may therefore be involved in the pathogenesis of gluten enteropathy.
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PMID:Histamine and mucosal mast cells in gluten enteropathy. 372 11

A 50-year-old male presented with intractable ascites due to systemic mastocytosis. The diagnosis of systemic mastocytosis was established by histology of the bone marrow which showed mast cell infiltration and fibrosis. Ascites was related to portal hypertension which was documented by esophageal varices at endoscopy and by an increase of wedged-free hepatic venous pressure gradient. Liver biopsy disclosed dense fibrosis of hepatic arterial and portal venule walls, resulting in complete obstruction of some portal radicles. Peliosis hepatis and fibrous deposits in the walls of hepatic venules were also present. Because of intractable ascites and significant malnutrition, a portacaval shunt was performed which cleared ascites and dramatically improved the general condition of the patient.
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PMID:Intractable ascites in systemic mastocytosis treated by portal diversion. 380 46

To determine the effects of protein malnutrition on the severity and duration of infection with Giardia lamblia, Mongolian gerbils were pair-fed a pelleted control (C) diet (20% protein) and a low-protein (5%; LP) diet for 3 weeks before and after being infected with 100,000 cysts orally. Weight loss, fecal fat, enteropooling, and the duration of cyst excretion were all greater in the infected LP than in the infected C animals. During peak infection the upper intestinal intraepithelial lymphocyte infiltration, crypt enlargement, and villus enterocyte migration were greater in C than in LP animals, as was the villus mast cell number at the end of the infection. It is concluded that in the protein-malnourished host the increased severity of Giardia infection correlates with a reduction in enterocyte production and migration, probably secondary to a reduced lymphocyte infiltration, and the increased infection duration correlates with blunted mast cell migration into affected villi.
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PMID:Effects of protein malnutrition on experimental giardiasis in the Mongolian gerbil. 826 17

Protein malnutrition may increase susceptibility to gastrointestinal parasitic infections, possibly as a result of impaired intestinal and/or systemic T helper 2 (Th2) effector responses induced by down-regulation of Th2 cytokines and/or up-regulation of Th1 cytokines. To test this hypothesis, female BALB/c mice (n = 18/diet) were fed a control (24%), marginal (7%), or deficient (3%) protein diet and given a challenge infection with Heligmosomoides polygyrus. The 3% mice had higher worm burdens at 1, 2, and 4 weeks postchallenge infection (pci), lower increases in serum IgE, reduced intestinal eosinophilia, and depressed mucosal mast cell proliferation and activation at 1-2 weeks pci. To determine whether these suppressed effector responses resulted from altered spleen and mesenteric lymph node (MLN) cytokine production, cells were restimulated in vitro with parasite antigen and cytokine concentrations were measured. Deficient MLN cells secreted significantly less IL-4 and more IFN-gamma at 1-2 weeks pci than did control MLN cells. Deficient spleen cells also secreted more IFN-gamma at 2 weeks pci compared with control spleen cells. From reverse transcription-PCR analyses, the 3% mice also had lower IL-4 mRNA level in spleen and MLN at 1-2 weeks pci. Our study supports the hypothesis that protein malnutrition increases the survival of a nematode parasite by decreasing gut-associated IL-4 (Th2) and increasing IFN-gamma (Th1) within 2 weeks pci, leading to reduced intestinal and systemic Th2 effector responses.
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PMID:Suppressed T helper 2 immunity and prolonged survival of a nematode parasite in protein-malnourished mice. 1086 Sep 74

Mastocytosis encompasses a range of disorders characterized by overproliferation and accumulation of tissue mast cells. Mast cell disease is most commonly seen in the skin, but the skeleton, gastrointestinal tract, bone marrow, and central nervous system may also be involved. We present a 10-year-old boy with diffuse cutaneous mastocytosis characterized by disseminated papular, nodular, and infiltrated leathery lesions. The patient presented with chronic diarrhea and malnutrition. Laboratory studies were normal except for an elevated urinary 1-methylhistamine level. The bone marrow aspirate showed a dense mast cell infiltrate confirming systemic involvement.
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PMID:Diffuse cutaneous mastocytosis with bone marrow infiltration in a child: a case report. 1088 51

While severe protein energy malnutrition (PEM) has been known to depress several immune functions, allergies are suppressed by decreasing IgE and impairing vascular permeability and mast cell functions. To address the effect of moderate protein malnutrition without growth arrest and protein hypernutrition on type I allergy, we examined the effect of various levels of protein nutrition on allergy at humoral immunity and the regulation of Th cell function levels. Mice fed 100 g/kg (moderate protein malnutrition; MPM), 200 g/kg (normal protein nutrition; PN) and 400 g/kg (protein hypernutrition; PH) protein diets were intraperitoneally sensitized to ovalbumin (OVA) in aluminum hydroxide. Higher elevations of OVA-specific IgE and total IgE in the serum were observed in the PH group as compared to the PN group. However, OVA-specific IgE in the MPM group was not significantly different from that in the PN group, although the former appeared higher than the latter. While CD3, CD4, CD8 and B220 expressions in the splenic lymphocytes were decreased in the MPM group, B220 expressions were increased in the PH group. Splenic lymphocyte proliferative responses to OVA were augmented in the PH group and depressed in the MPM group. IFN-gamma production from splenic lymphocytes was significantly decreased; however, IL-4 production was not affected significantly in the MPM group, and increased in the PH group. These findings suggest that immune functions to specific antigens in the MPM state are depressed at the cytokine level but not in terms of IgE responses. They also suggest that immune functions become Th2-predominant in the PH state, resulting in an increased risk of type I allergy.
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PMID:IgE responses in mice fed moderate protein deficient and high protein diets. 1295 95

Lysosomal carboxypeptidase A (cathepsin A) is synthetized in the form of preproenzyme, which undergoes to active enzyme as a result of post-translational modification. It splits off C-terminal amino acid residues from peptides and proteins and synergizes with other proteases in degradation of cellular proteins in lysosomes. Lysosomal carboxypeptidase A has an effect on peptide hormones and peptides of biological activity of tissues and body fluids as well. It forms complexes with some glycosidases that protects them against proteolytic degradation. Deficiency of this enzyme induces storage diseases. Lysosomal carboxypeptidase A as multifunctional enzyme plays an important regulatory role in organismal metabolism.
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PMID:[Lysosomal carboxypeptidase A]. 1620 54


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