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)

Lymphocytes of the mouse intestinal mucosa, identified in tissue sections or purified suspensions of intraepithelial lymphocytes as T cells (gut T lymphocytes [GTL]), were studied in normal mice or in beige mice (the equivalent of the Chediak-Higashi syndrome in man, characterized by giant granules in various cell types, including mast cells). Mice were studied in normal or in germ-free conditions, or during a graft versus host (GVH) reaction resulting from the injection of parental thymocytes into lethally irradiated F1 mice, a condition leading to massive accumulation of T lymphocytes of donor origin in the host gut mucosa. In normal as well as in GVH conditions, a high percentage of the gut IE lymphocytes contain granules (up to 80% in the beige mouse). These granules have ultrastructural, hostochemical and other features resembling those of mast cell granules; in beige mice, up to 50% of them can be shown to contain histamine. Granulated T cells are also found in the lamina propria. It appears that the GTL may progressively lose their surface T antigens when the granules become more developed. Kinetics of [3H]TdR labeling of the GTL, transfer experiments with T cells of various origins, selective [3H]TdR labeling and selective irradiation of the Peyer's patches (PP), and effect of thoraic duct (TD) drainage led to the conclusion that GTL are the progeny of T cells stimulated to divide in the PP microenvironment, which endows them with a gut-homing tendency. From the PP, these cells follow a cycle, migrating to the TD and to the blood to colonize the whole intestinal mucosa, the majority of them as dividing cells undergoing a single round of traffic, with some probably able to recirculate and becoming a more long-lived variety. Antigenic stimulation within the PP is necessary for the emergence of GTL progenitors, but their gut-homing property is unrelated to the antigen as shown with fetal gut grafts, notably in GVH where grafts syngeneic to the host or donor become similarly infiltrated by GTL. On the basis of their properties and of further evidence to be reported elsewhere, it is proposed that GTL belong to a special class of T lymphocytes, related to the immune defenses of the mucosal systems in general, and capable of acting as progenitors of mucosal mast cells.
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PMID:The mouse gut T lymphocyte, a novel type of T cell. Nature, origin, and traffic in mice in normal and graft-versus-host conditions. 3 10

We have previously reported that intestinal mast cells represent a separate population of mast cells which is thymus- (T-) dependent. In this paper we examine whether the appearance of these cells is dependent on thymus-dependent antibodies or thymus serum factor(s). The response of intestinal mast cells and globule leucocytes to a Trichinella spiralis infection was therefore studied in congenitally athymic (nude) mice after treatment with specific anti-T. spiralis hyperimmune serum or normal mouse serum from thymus-bearing litter-mates. However, transfer of both types of serum did not lead to an intestinal mast cell response. It was concluded that the presence of an intact thymus or T-dependent cellular reactions and/or their products are essential for appearance of intestinal mast cells. In contrast infected athymic mice reacted with a minor reponse of globule leucocytes irrespective of the serum transfer. Occasionally metachromatic intra-epithelially located cells with toluidine-blue-positive granules, believed to be globule leucocytes, showed mitotic figures. Metachromatic cells were observed occasionally within the lumen of the gut. These data were interpreted as supporting the idea that the globule leucocyte is a cell sui generis and independent of the intestinal mast cell.
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PMID:Response of intestinal globule leucocytes in the mouse during a Trichinella spiralis infection and its independence of intestinal mast cells. 31 2

The gut wall is one of the conspicuous sites of eosinophil accumulation, presumably because of local chemotactic stimuli. It is reasonable to assume that one chemotactic factor is released by the mast cell, which is often found in proximity to the eosinophil. The association of eosinophils and eosinophilia with allergic disorders has long been recognized, and recent work has shown that increased eosinophil production is mediated by the lymphocyte. That process shares characteristics with other immunological actions. An increased rate of eosinophil tissue accumulation and destruction may be the factor which initiates the mechanism for increased production. None of many hypotheses about the 'function' of the eosinophil is substantiated; nevertheless it seems likely that this member of the immunological apparatus, which tends to be distributed in the front line (mucosal and cutaneous tissues), fulfils some normal protective or homeostatic function. Aside from that assumed normal function, there is growing clinical evidence that eosinophils can at times cause host injury, for example in such states as eosinophilic gastroenteritis and endomyocarditis.
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PMID:Immunology of the gut: role of the eosinophil. 34 22

The alterations of mast cell counts induced in the gut of swiss albino mice by infection with Ancylostoma caninum larvae have been studied, both in single and multiple infections. It was found that mast cell rise was greater in females than males. In singly infected animals, mast cell increase was influenced by the infective dose of inoculated larvae. In case of repeatedly infected mice, mast cell counts were decreased because of their earlier degranulation.
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PMID:Intestinal mast cells during experimental ancylostomiasis. 45 29

A comparative autoradiographic study on the uptake and intracellular localization of 3H-leucine-, 3H-dopa-, 3H-dopamine- and 3H-ATP-derived radioactivity was performed in the mouse carotid body to investigate the metabolic features of the chief cell as a paraneuron. 3H-leucine-derived radioactivity representing recently synthesized peptides was demonstrated in all kinds of cells in the carotid body and surrounding area. The chief cell was less radioactive than the nerve cell in the superior cervical ganglion. In the electron microscope autoradiography, no accumulation of radioactivity could be demonstrated either in the Golgi area of the chief cell, where the membrane-bound particles were probably formed, nor in the periphery of the cells, where they were stored before their release. Incorporation of 3H-dopa-derived radioactivity representing recently synthesized catecholamines was specific to the chief cell, mast cell, and nerve cell in the superior cervical ganglion. In the chief cell the distribution of radioactivity was roughly identical with that of the large dense-cored vesicles. Striking accumulations of 3H-dopamine-derived radioactivity were demonstrated in the adrenergic nerve terminals in the perivascular space and the glomus complexes of the carotid body. Not all of the chief cells incorporated the 3H-dopamine-derived radioactivity. 3H-ATP derived radioactivity was demonstrated in all kinds of cells in the carotid body and surrounding tissues. In the chief cell, as in other kinds of cells, the highest radioactivity was seen in the nucleus. The present results suggest that, if the large dense-cored vike those membrane-bound particles in other paraneurons, contain peptides, monoamines and ATP, the turnover of these products as secretory materials is much slower in this cell than in such endocrine paraneurons as adrenal chromaffin cells and gut endocrine cells.
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PMID:An autoradiographic study of the mouse carotid body using tritiated leucine, dopa, dopamine and ATP with special reference to the chief cell as a paraneuron. 102 Oct 15

There is mounting evidence for interactions between the immune and peripheral nervous systems. Many regulatory molecules are candidate mediators for communication between inflammatory cells and nerves; however, the extent of targeting of neurotransmitters (and interleukins) as intersystem messengers has been somewhat overlooked. Lymphoid tissues are well supplied by nerves and the gastrointestinal lamina propria, which is populated by a variety of immune cell types, is densely innervated. One-half to two-thirds of mast cells are closely apposed to nerves in the intestinal mucosa, in both rodents and humans, and nerve stimulation has been reported to cause mast cell activation. Although less extensively studied, both eosinophils and plasma cells in the gastrointestinal mucosa are also positioned for interaction with nerves, and intra-epithelial leukocytes may be subject to diffusible neurally-derived mediators. Peyer's patches are relatively sparsely innervated but appear to express neuropeptide receptors in inflammatory conditions. Although the nerves in the mucosa have traditionally been thought of as a static component, recent experiments suggest that these may undergo extensive remodelling during nematode-induced inflammation. Such data suggest a dynamic interplay between the immune and nervous systems during inflammatory episodes in the gut, although considerable work is still needed to determine the importance of neuro-immune interactions in gastrointestinal homeostasis and inflammation.
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PMID:Innervation of mucosal immune cells in the gastrointestinal tract. 135 71

Changes in the activities of three gastric and nine pancreatic enzymes plus colipase were determined during postnatal development and weaning in calves. In calves exclusively milk-fed for 2, 7, 28, 56, 70 and 119 d, the enzyme activities per kilogram of empty live weight increased with age for chymotrypsin, elastase, carboxypeptidases A and B, ribonuclease and alpha-amylase, decreased for chymosin, lysozyme and colipase but showed no change in the case of pepsin, trypsin, lipase and phospholipase A2 compared with animals at birth. The greatest increase was that in alpha-amylase activity (about 50-fold between d 2 and 119). In calves weaned between d 28 and 56, all the activities were higher than in milk-fed animals, except that of chymosin (which was slightly lower) and that of colipase (which did not change). At 119 d of age, chymotrypsin, carboxypeptidase A, alpha-amylase and lipase were 1.6- to fourfold higher in ruminants than in preruminants. Thus, most enzyme activities were modified first by colostrum and milk intake, and again upon weaning by development of the forestomachs and ingestion of solid food. These ontogenic patterns might be under the control of many gut regulatory peptides, the plasma concentrations of which changed simultaneously. Some gastric and pancreatic enzymes were correlated to plasma concentrations of these gut regulatory peptides.
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PMID:Gastric and pancreatic enzyme activities and their relationship with some gut regulatory peptides during postnatal development and weaning in calves. 137 46

The mast cell, equipped with enzymes, chemotactic factors, a vasoactive amine, an anticoagulant, and lipid-derived proinflammatory products, may be essential in tissue modeling as well as in defense. Its primarily perivascular location in skin and the mucosa of the respiratory tract and the gut assures its availability to counter parasites. By the same token, the mast cell is responsible for interactions with inhaled, ingested, and injected antigens that comprise IgE-mediated allergic reactions. Abnormally high numbers of mast cells in the skin, either localized or generalized, result in urticaria pigmentosa or generalized cutaneous mastocytosis, respectively. Tissue infiltration by excessive mast cells, primarily in gut, bone, liver, and spleen, results in systemic mastocytosis; this may be accompanied by myelodysplasia or lymphoma and may eventuate in mast cell leukemia. Until the etiology of mastocytosis is understood, the treatment is symptomatic: histamine antagonism by H1 +/- H2 blockade for flushing, itching, and gastric distress; cyclooxygenase inhibition to prevent prostaglandin D2 (PGD2)-induced hypotension when indicated; and oral cromolyn to prevent gastrointestinal symptoms and bone pain.
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PMID:Mast cell disease. 149 Jun 22

Mast cells are a significant component of the mucosa in the gastrointestinal tract. There is increasing evidence that these cells are involved in the pathophysiology of various intestinal disorders ranging from food allergy to inflammatory bowel disease. When activated, mast cells release a host of potent mediators and cytokines which are capable of inducing pathophysiology. The bulk of the evidence has come from hypersensitivity studies in experimental animals sensitized either by parasitic infection or by active immunization to an antigen using adjuvants which stimulate IgE production. Subsequent antigen challenge of the gut results in mast cell activation associated with alterations in intestinal functions including ion transport and epithelial permeability. Intestinal secretory transport responses are inhibited by antagonists of mast cell mediators and neurotoxins, implicating mast cell-nerve interactions with the epithelium. In genetically mast cell-deficient mice, antigen-induced secretion is reduced approximately 70% and this component is not affected by neural or mast cell inhibitors; adoptive transfer of bone marrow containing mast cell precursors derived from congenic normal mice restores the complete antigen response. These results provide more direct proof that mast cell activation causes abnormal gut function. Recently, we have begun studies which indicate that activation of mast cells induces ion secretion in surgically resected human intestine. Reduced secretory responses in specimens from patients with IBD suggest that mast cells may play a role in the pathophysiology of inflammatory bowel disease.
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PMID:Functional abnormalities in the intestine associated with mucosal mast cell activation. 150 88

We examined the distribution and functional integrity of mast cells in intestinal longitudinal muscle in rats sensitized by two previous infections with Trichinella spiralis. A segment of jejunum was excluded from the gut before infection, and the remainder of the gut was anastomosed. Few mast cells were seen in muscle of noninfected control rats except in the region of the jejunal anastomosis. In rats sensitized by T. spiralis infection, mast cells were increased in number in the jejunum and the number of mast cells followed an aboral gradient down the entire length of the gut in continuity. In addition, mast cells were present in muscle of the excluded segment of sensitized rats. All mast cells were stained red with safranin. Functional integrity was assessed by the ability of mast cells to induce contraction after degranulation by antigen. In muscle from sensitized rats, contraction was induced in each region after exposure to T. spiralis antigen but not Nippostrongylus brasiliensis antigen. Contraction was inhibited by the mast cell stabilizer doxantrazole and the 5-hydroxytryptamine (5-HT) antagonist cyproheptadine. When antigen-induced contraction was expressed as a percentage of the maximum response of the tissue to exogenous 5-HT, the magnitude of contraction decreased along an aboral gradient down the intestine and correlated well (r2 = 0.878) with mast cell numbers. These results suggest that the increase in connective tissue mast cells in gut muscle after T. spiralis infection involves both local and systemic mechanisms.
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PMID:Distribution of mast cells in intestinal muscle of nematode-sensitized rats. 155 Feb 36


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