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)

We tested the hypothesis that mast cells contribute to platelet-activating factor (PAF)-induced airways hyperreactivity and hyperpermeability in mice. Airways reactivity to acetylcholine (ACh) and lung permeability to Evans blue (EB) dye were measured before and after PAF challenge in genetically mast cell-deficient (WBB6F1 W/Wv) and normal congenic (WBB6F1 +/+) mice, as well as mast cell-reconstituted (BMT W/Wv) mice. In addition, prostaglandin D2 (PGD2), a mast cell-specific mediator, was measured in the bronchoalveolar lavage (BAL) from +/+ and W/Wv mice to determine if lung mast cell activation was a consequence of PAF challenge. Genetically PAF-sensitive AKR/J mice were also treated with the mast cell stabilizer nedocromil prior to assessment of PAF effects on ACh reactivity. Intravenous PAF (10 micrograms/kg) induced a significant (P < 0.05) increase in airways reactivity to ACh (25 micrograms/kg) in both +/+ (371 +/- 52%) and W/Wv (122 +/- 24%) mice. There was a significantly greater increase in +/+ compared with W/Wv mice. PAF-induced hyperreactivity to ACh in BMT W/Wv mice (191 +/- 44%) was significantly (P < 0.05) greater than age-matched W/Wv mice (80 +/- 16%), but not significantly different from age-matched +/+ mice (153 +/- 44%). PAF (10 micrograms/kg) also significantly (P < 0.5) increased lung permeability in +/+ and W/Wv mice, but there was no significant difference between groups. BAL PGD2 increased significantly in +/+ mice following PAF challenge (559 +/- 24 ng/ml) compared with vehicle controls (152 +/- 8 pg/ml). There was no significant increase in BAL PGD2 from W/Wv mice. Nedocromil pretreatment significantly (P < 0.05) decreased PAF-induced hyperreactivity in AKR/J mice but not in W/Wv mice (P > 0.05). We conclude that mast cells contribute significantly to PAF-induced hyperreactivity but not hyperpermeability in mice.
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PMID:PAF-induced airways hyperreactivity is modulated by mast cells in mice. 862 51

Airways inflammation and epithelial injury induced by chronic ozone (O(3)) in genetically mast cell-deficient mice (Kit(W)/Kit(W-v)) were compared with those in mast cell-sufficient mice (+/+) and Kit(W)/Kit(W-v) mice repleted of mast cells (Kit(W)/Kit(W-v)-BMT). Mice were exposed to 0.26 ppm O(3) 8 h/day, 5 days/wk, for 1-90 days. Background was 0.06 ppm O(3). Age-matched mice were exposed to filtered air for O(3) controls. Reversibility of lesions was evaluated 35 days after exposure. Compared with Kit(W)/Kit(W-v), O(3) caused greater increases in lavageable macrophages, epithelial cells, and polymorphonuclear leukocytes in +/+ and Kit(W)/Kit(W-v)-BMT mice. O(3) also caused lung hyperpermeability, but the genotypic groups were not different. Cells and permeability returned to air control levels after O(3). O(3) induced lung cell proliferation only in +/+ and Kit(W)/Kit(W-v)-BMT mice; proliferation remained elevated or increased in +/+ and Kit(W)/Kit(W-v)-BMT mice after O(3). Greater O(3)-induced cell proliferation was found in nasal epithelium of +/+ and Kit(W)/Kit(W-v)-BMT mice compared with Kit(W)/Kit(W-v) mice. Results are consistent with the hypothesis that mast cells affect airway responses induced by chronic O(3) exposure.
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PMID:Airway responses to chronic ozone exposure are partially mediated through mast cells. 1116 73

Atherosclerosis is an inflammatory disease characterized by the influx of macrophages and T cells and IL-17 may connect innate and adaptive immune responses involved in atherogenesis. We investigated the role of IL-17 receptor signaling in atherosclerosis and transplanted LDLr deficient recipient mice with IL-17R deficient bone marrow. Induction of atherosclerosis by Western-type diet induced a 46% reduction in lesion size in the aortic root and the plaque composition revealed no significant changes in collagen content and neutrophil counts, but a reduction in mast cell number and an increase in macrophage number. In addition, we observed a decrease in anti-oxLDL antibodies of the IgG class upon IL-17R BMT, while introduction of IL-17R deficient bone marrow resulted in a reduced IL-6 production and an increased IL-10 production. In conclusion, signaling via the IL-17 receptor in bone marrow derived cells enhances the process of atherosclerosis.
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PMID:Attenuated atherosclerosis upon IL-17R signaling disruption in LDLr deficient mice. 1966 Apr 32