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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our knowledge on immunopathogenic damage is derived from multiple different sources: experiments in vitro, experiments in vivo, clinical observations, and observations using material from multiple different animal species including man. If we want to analyse an immunological process suspected of causing tissue damage we have critically to evaluate the mechanism of immunologically specific initiating factors and the mechanisms of non-specific mediating factors. It is necessary to have clear information on the identity of the antigen, the location of the antigen, the identity of antibody, the location of antibody and similar information on specifically reactive lymphocytes. With this information in mind it is possible to hypothesize upon mechanisms, which can be responsible for the immunologically specific initiation of immuno-pathogenic damage. The non-specific mediating systems, which are the actual inducers of functional or structural tissue damage, are triggered by the specific, initial immune reaction. These systems comprise for instance complement, coagulation, granulocyte and macrophage lysozomes and function, chemotaxis, the mast cell system, phagocytosis etc. The overall picture of non-specific mediation of tissue damage is extremely complex, since it really makes it necessary to investigate and describe not only these systems but also their co-existence and interaction. Knowledge of immunopathogenic mechanisms in clinical disorders in man is still resting mainly upon analogies and assumptions, although progress is taking place. It is essential to ask the right questions and critically to evaluate the answers. Thereby the understanding of immunopathogenesis in diabetes mellitus and other clinical disorders shall gradually improve.
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PMID:Immunopathogenic mechanisms in tissue damage. 6 10

Rat mortality and contractile responses of isolated tracheas to compound 48/80 from rats made diabetic 4 days before by a single intravenous injection of alloxan and from diabetic rats that had been treated with insulin 6 h before were compared with control animals. Diabetic animals and tracheal segments from diabetic rats were significantly less responsive to compound 48/80 than control and insulin-treated diabetic animals. On the other hand, diabetic animals have a lower quantity of peritoneal mast cells than control rats, and insulin restored the normal quantity of cells in diabetic animals. These data indicate that diabetes elicits an hyposensitivity to compound 48/80, possibly related to a diabetes-induced decrease in the mast cell count.
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PMID:Diabetes-induced rat hyposensitivity to compound 48/80. 191 34

The flare response in skin largely depends on an intact primary sensory fiber, the C-fiber. We measured the flare response to the intradermal injection of substance P, histamine, and capsaicin in control subjects and in diabetic patients with and without clinically obvious polyneuropathy. The neuropathic diabetic patients had a reduced flare response to substance P, histamine, and capsaicin, compared with control and nonneuropathic diabetic subjects. The smaller flare response in the neuropathic diabetics after capsaicin administration suggested a dysfunction of the peripheral component of the C-fiber. Alternatively, dysfunction of the mast cell or vascular reactivity may contribute to the diminished flare. Because C-fibers participate in nociception in addition to the flare response, the findings of this study, by a method that permits a quantifiable measurement of the function of peripheral sensory neurons in diabetic subjects, has potential usefulness in evaluating sensory neuropathy in diabetic patients.
Diabetes 1987 Oct
PMID:Diminished flare response in neuropathic diabetic patients. Comparison of effects of substance P, histamine, and capsaicin. 244 7

We have previously reported that rats which have been suffering from streptozotocin-diabetes for 4 weeks show a supranormal mast cell mediated mitogenesis in mesenteric windows and in the skin; this late emerging, augmented mitogenic responsiveness appears, to be unaffected by insulin per se. To test whether this increased proliferogenic response is effected by some acquired quality within the tissue rather than a systemic factor in the blood, we studied mast cell mediated mitogenesis in organ-cultured intact mesenteric windows from rats with diabetes of 4 weeks' duration, using a biochemically-defined serum-free growth medium. Mast cells were activated by Compound 48/80 and their secretion was quantified biochemically in terms of histamine release. The mast cell-dependent mitogenic reaction in the predominant, morphologically discrete fibroblasts and mesothelial cells was quantified photometrically using Feulgen-absorption analysis of individual cell nuclei, and by determination of the mitotic index. Both types of target cell responded to a significantly greater degree mitogenically in diabetic compared with control tissue. This finding suggests that a considerable part of the increased mitogenic responsiveness previously observed in diabetic animals in vivo is causally related to some tissue-bound, i.e., cellular and/or extracellular factor(s) acquired during the course of the disease.
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PMID:Evidence of an acquired increase in mitogenesis in streptozotocin-diabetic rats, apparently relating to some tissue factor. 256 25

A single high dose of streptozotocin was found to cause a transient increase in islet capillary permeability 2-4 h after administration. Staining of areas of increased vascular permeability by Evans blue showed that islets, but not exocrine tissue, were affected. The permeability increase seems to involve vasoactive substances released by mast cells. A mast cell inhibitor (disodium cromoglycate) and a serotonin antagonist (methysergide) were found protective. Furthermore, administration of methysergide partially prevented the development of hyperglycaemia in streptozotocin-treated rats. In mice, almost full protection from diabetes development was reached by both methysergide and disodium cromoglycate. Our observations indicate an important role of mast cell controlled membrane permeability in this model of beta-cell destruction and diabetes development.
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PMID:Diabetogenic action of streptozotocin: essential role of membrane permeability. 294 74

Transplantation of cultured islet and pituitary tissue from PVG (RT1c) donors to major histocompatibility complex-incompatible BB/D recipients (RT1u) results in tissue-specific destruction of the grafted islets but not of the pituitary. We interpret this response as disease occurrence in the MHC-incompatible islet graft. Islet damage is associated with eosinophil and mast cell accumulation in and around the grafted tissue. Antibody deposition is also present in tissues of the BB rat. This is suggestive of an antibody-mediated allergic reaction.
Diabetes 1986 Jan
PMID:Islet allografts are destroyed by disease occurrence in the spontaneously diabetic BB rat. 307 13

Mast cells around the thymus of rats stain red with alcian blue and safranin indicating that the mast cells are probably of the peritoneal (connective tissue) type. After the onset of streptozotocin induced diabetes some cells contain both red and blue granules and blue staining cells may appear. X-ray microanalysis of frozen freeze-dried sections from diabetic male CSE Wistar rats showed electron dense granules to have similar amounts of S to normal rat mast cell granules but reduced levels of Na, Mg, P, Cl and K. Two cells also had electron lucent granules with very high levels of Na, Cl, K and Ca and reduced concentrations of S. The differences in elemental composition suggest that the mast cells from diabetic rats are not immature, but are related to the condition of induced diabetes, and that granules of very different composition can occur within a single cell. X-ray microanalysis has given an insight into mast cell granule elemental content which was not possible by conventional biochemical methods.
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PMID:Elemental levels in mast cell granules differ in sections from normal and diabetic rats: an X-ray microanalysis study. 336 63

Rats with diabetes of 4 weeks' duration have previously demonstrated increased mitogenesis in normal connective tissue cells following mast cell secretion. The appearance of this augmented mast cell-mediated mitogenic reactivity was studied in the mesentery of insulin-deficient rats, 3, 7, and 28 days after they had been rendered diabetic by a single dose of streptozotocin. On day 7 mast cell secretion induced a subnormal mitogenic response which, however, increased above normal on day 28. This time lag in the augmentation of mitogenic responsiveness may be important since proliferative lesions in diverse mesenchymal tissues typically develop with a similar delay in both experimental and clinical diabetes.
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PMID:Delayed mast cell mediated mitogenic reactivity in diabetic rats. 613 82

Proteolytic enzyme activities were measured in skeletal muscle of Sprague-Dawley rats with streptozotocin-induced diabetes [tail vein injection of streptozotocin (100 mg/kg), under ether anesthesia]. Assay of rat muscle homogenates from diabetic rats revealed a significant increase in alkaline serine protease activity as compared to untreated control rats and diabetic rats given insulin. There were no significant changes in lysosomal cathepsin activities in diabetic muscle as compared to controls. Gel studies of myofibrils isolated from the three groups of rats, subjected to autolysis, revealed that the serine protease had copurified with the myofibrils. Treatment of rats with compound 48/80, which degranulates mast cells, abolished the alkaline protease activity. There was no serine protease activity associated with the myofibrils isolated from compound 48/80-treated rats. Results from this study indicate that serine proteases are not involved in muscle protein breakdown in diabetes and are of mast cell origin.
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PMID:Muscle proteolytic enzyme activities in diabetic rats. 703 84

Mast cell proliferation has been reported in peripheral nerves of streptozotocin diabetic rats. We examined the question by light microscopy using morphometric techniques including estimation of shape and size. After 4 weeks of diabetes the mast cell area in transverse sections was 32.7 +/- 7.0 microns 2 vs. 22.5 +/- 5.4 microns 2 in controls (P less than 10(2)). Mast cell profiles approximated to ellipses in longitudinal sections, the long diameter being 11.4 +/- 1.2 microns vs. 14.0 +/- 1.0 microns in controls (P less than 10(4)). Correspondingly, the profile number was increased (30 +/- 6%) in longitudinal sections and decreased in transverse sections (11 +/- 16%). The present study does not provide evidence for mast cell proliferation in peripheral nerves in experimental diabetes, and, furthermore, underlines the need of evaluation of dimensions in studies of particle numbers.
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PMID:Change in mast cell dimensions increases the profile number in sections of peripheral nerve of diabetic rats. 706 65


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