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

The enteric nervous system in the small intestine of cattle during Schistosoma bovis infection was studied by histological stains and immunohistochemical methods. Lesions due to migration of schistosoma eggs were located mainly in the mucous and the submucous layer overlaying the submucous vascular arcades. Granulomas destroyed ganglia, neurons, nerves fibre strands and nerve fibres. Ganglia situated within or near granulomas were infiltrated by mast cells, eosinophils, lymphocytes, globule leukocytes, neutrophils and macrophages. Mast cells were in close contact with degenerating neuronal perikarya. Whereas vasoactive intestinal peptide-like immunoreactivity in the nerves and neurons in the ganglia within and around granulomas was increased, the neurofilament-like immunoreactivity was reduced. Compared to the myenteric and external submucous plexuses, the internal submucous and mucous plexuses were the most damaged. These changes imply reduced functional capacity in the nervous tissue which might cause reduced motility, malabsorption and partly account for the loss of body weight and condition and failure to thrive which occur in schistosomosis. Biotinylated affinity purified swine anti-rabbit and mouse anti-rabbit immunoglobulins reacted nonspecifically with a subset of mast cells. The reaction revealed many mast cells in early forming granulomas and around schistosome egg tracts and infiltration of mast cells into the ganglia of intestinal nerve plexuses. The observation shows a localized, Type I hypersensitivity reaction suggesting for the release of mast cell-derived chemical mediators in the intestinal reaction to trap or evict S. bovis eggs and to cause diarrhoea.
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PMID:Lesions of the enteric nervous system and the possible role of mast cells in the pathogenic mechanisms of migration of schistosome eggs in the small intestine of cattle during Schistosoma bovis infection. 1082 12

Eosinophilic esophagitis (EoE) is a disorder of increasing prevalence worldwide, causing clinical symptoms of vomiting, failure to thrive, and dysphagia and complications of esophageal remodeling with strictures and food impactions. Molecular profiling demonstrates EoE to be an eosinophil-predominant disorder with a TH2 cytokine profile reminiscent of other allergic diseases, such as asthma, allergic rhinitis, and atopic dermatitis. Environmental antigens in the form of foods and aeroallergens induce eosinophil, basophil, mast cell, and T-cell infiltration. Pathogenesis depends on local epithelial immune activation with production of thymic stromal lymphopoietin and eotaxin-3. Complications mirror asthmatic airway pathogenesis, with increases in subepithelial collagen deposition, angiogenesis, and smooth muscle hypertrophy. The removal of instigating antigens, especially foods, causes disease resolution in more than 50% of adults and children. The prevalence of concurrent atopic disorders in patients with EoE and the need to control antigen-specific TH2 inflammation underscore the importance of testing for allergens and treating the entire atopic subject to control the potential interplay between organ-specific allergic responses.
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PMID:Allergic components of eosinophilic esophagitis. 2998 Feb 77