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)

Airway smooth muscle cells (ASMC) play a major role in airway inflammation, hyperresponsiveness, and obstruction in asthma. However, very little is known regarding the relation between inflammatory mediators and cytokines and immature ASMC. The aim of this study was to evaluate 1) the secretion of leukemia inhibitory factor (LIF) (an IL-6 family neurotrophic cytokine) by ASMC; 2) intracellular calcium concentration ([Ca(2+)](i)) signaling; and 3) the effect of LIF on mast cell chemotaxis and rat airway contractility. Immature and adult human ASMC were cultured. ELISA and real-time PCR were performed to assess LIF protein secretion and mRNA production, [methyl-(3)H]thymidine incorporation to quantify ASMC DNA synthesis, a Boyden chamber to evaluate the effect of LIF on mast cell chemotaxis, microspectroflurimetry using indo-1 (at baseline and after stimulation bradykinin, U-46619, histamine, and acetylcholine, in the presence or absence of LIF or TNF-alpha) for [Ca(2+)](i) signaling, and isolated rat pup tracheae to determine the effect of LIF on airway contractility to ACh. TNF-alpha-stimulated immature ASMC produce more LIF mRNA and protein than adult ASMC, although this cytokine induces a moderate increase in DNA synthesis (+20%) in adult ASMC only. Human recombinant LIF exerts no chemotactic effect on human mast cells. In immature ASMC, ACh-induced [Ca(2+)](i) response was enhanced twofold after incubation with LIF, whereas TNF-alpha increased the [Ca(2+)](i) to U-46619 threefold. In TNF-alpha-exposed adult ASMC, [Ca(2+)](i) responses to ACh were of greater magnitude (sixfold increase) than in immature ASMC. Human recombinant LIF increased contractility to ACh by 50% in immature, isolated rat tracheae. Stimulated immature human ASMC greatly secrete LIF, thus potentially contributing to neuroimmune airway inflammation and subsequent remodeling. Increased LIF secretion enhances airway reactivity and [Ca(2+)](i) signaling.
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PMID:Increased secretion of leukemia inhibitory factor by immature airway smooth muscle cells enhances intracellular signaling and airway contractility. 1648 16

BACKGROUND This study evaluated the anti-allergic activity of corilagin and also postulates the possible mechanism of its action. MATERIAL AND METHODS Corilagin was given orally at dose of 10, 20, and 40 mg/kg/day. All the animals (guinea pigs, rats, and mice) were sensitized for allergy such as eosinophilia and leukocytosis induced by milk; degranulation of mast cell by compound 48/80; and passive and active anaphylaxis. Moreover, the antagonistic effect was determined by estimating the effect of corilagin on contraction of guinea pig tracheal chain and ileum induced by Ach and histamine, respectively. RESULTS There was a significant decrease in the leukocyte and eosinophil counts in the corilagin-treated group compared to the negative control group. Treatment with corilagin significantly protects the degranulation of mast cells, and it also has significant anti-muscarinic and antihistaminic activity by reducing the muscle contraction induced by Acetylcholine (Ach) and histamine in guinea pig tracheal chain and ileum. CONCLUSIONS Corilagin possess anti-anaphylactic and anti-allergic activity by inhibiting the release of mediators from mast cells and by decreasing the serum concentration of immunoglobulin E (IgE).
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PMID:Corilagin Attenuates Allergy and Anaphylactic Reaction by Inhibiting Degranulation of Mast Cells. 2943 82


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