In this study, total IgE and mast cell tryptase were measured in a series of forensic autopsy cases including non-allergic cardiac deaths (14 cases with minimal or no coronary atherosclerosis, 14 cases with significant coronary artery atherosclerosis without acute coronary thrombosis, and 14 cases with significant coronary artery atherosclerosis and acute coronary thrombosis or myocardial infarction) and non-allergic non-cardiac deaths (21 cases with death due to hanging and 21 cases with death due to intracranial gunshot wounds), in order to correlate laboratory results with morphological findings and compare them to conclusions reported in the clinical setting.
In this study, total IgE and mast cell tryptase were measured in a series of forensic autopsy cases including non-allergic cardiac deaths (14 cases with minimal or no coronary atherosclerosis, 14 cases with significant coronary artery atherosclerosis without acute coronary thrombosis, and 14 cases with significant coronary artery atherosclerosis and acute coronary thrombosis or myocardial infarction) and non-allergic non-cardiac deaths (21 cases with death due to hanging and 21 cases with death due to intracranial gunshot wounds), in order to correlate laboratory results with morphological findings and compare them to conclusions reported in the clinical setting.
The expression of tissue necrotic factor-α, vascular endothelial growth factor, CD31, transforming growth factor-β and SLUG was significantly increased in non-Hunner type interstitial cystitis and Hunner type interstitial cystitis patients compared with controls whereas the significant increases in the expression of mast cell tryptase and collagen were observed in Hunner type interstitial cystitis patients compared with controls and non-Hunner type interstitial cystitis patients.
The expression of tissue necrotic factor-α, vascular endothelial growth factor, CD31, transforming growth factor-β and SLUG was significantly increased in non-Hunner type interstitial cystitis and Hunner type interstitial cystitis patients compared with controls whereas the significant increases in the expression of mast cell tryptase and collagen were observed in Hunner type interstitial cystitis patients compared with controls and non-Hunner type interstitial cystitis patients.
Histopathological, immunohistochemical, and flow cytometry studies of the resection specimens showed the tumor to be mostly composed of CD117-positive and mast cell tryptase-positive cells with features consistent with mast cell sarcoma.
Bladder biopsies from patients with bladder pain syndrome/interstitial cystitis, including 12 with and 19 without Hunner lesions, 13 with overactive bladder syndrome and 12 healthy controls, were analyzed by immunohistochemistry with antibodies to the nerve cell marker PGP9.5 (neuron-specific protein gene product 9.5), p75<sup>NTR</sup> (p75 neurotrophin receptor), the B-lymphocyte marker CD20 and mast cell tryptase.
This study examined expression of PAR2 and endogenous proteinase activators (trypsin-2, mast cell tryptase) and proteinase inhibitors (serpin-A5, serpin-A13) in areas vulnerable and resistant to neurodegeneration in Parkinson's disease at different Braak α-synuclein stages of the disease in post-mortem brain.
Altered immunohistochemical expression of mast cell tryptase and chymase in the pathogenesis of oral submucous fibrosis and malignant transformation of the overlying epithelium.
Serine proteases such as trypsin and mast cell tryptase cleave protease-activated receptor-2 (PAR2) at R(36)↓S(37) and reveal a tethered ligand that excites nociceptors, causing neurogenic inflammation and pain.
Altered immunohistochemical expression of mast cell tryptase and chymase in the pathogenesis of oral submucous fibrosis and malignant transformation of the overlying epithelium.
We conclude that: 1) Hp infection is associated with a decreased risk for food allergy; 2) presence of Hp in food allergy patients has ameliorating effect on the production of allergy mediators such as ECP and mast cell tryptase and 3) Hp infection appears to be a protective factor against food allergy.
We conclude that: 1) Hp infection is associated with a decreased risk for food allergy; 2) presence of Hp in food allergy patients has ameliorating effect on the production of allergy mediators such as ECP and mast cell tryptase and 3) Hp infection appears to be a protective factor against food allergy.
Inflammatory proteases (mast cell tryptase and trypsins) cleave protease-activated receptor 2 (PAR2) on spinal afferent neurons and cause persistent inflammation and hyperalgesia by unknown mechanisms.
PAR-2-mediated intestinal electrolyte secretion by release of mast cell tryptase and potentiation of PAR-2 expression by tumor necrosis factor-alpha may contribute to the hypersecretion observed in inflammatory processes such as chronic inflammatory bowel disease.
These findings suggest that mast cell tryptase plays a role in the proliferation and extracellular matrix protein production of renal interstitial fibroblasts and thus contributes to the development of renal interstitial fibrosis.
These findings suggest that mast cell tryptase plays a role in the proliferation and extracellular matrix protein production of renal interstitial fibroblasts and thus contributes to the development of renal interstitial fibrosis.
Using specific antibodies to mast cell tryptase, tissue macrophage, and bFGF, we demonstrate that cytoplasmic bFGF immunoreactivity is localized to 96.8 +/- 9.6% of tryptase-positive cells in human fibrotic lung tissue (n = 10), 82.3 +/- 6.9% of tryptase-positive cells in rheumatoid synovia (n = 6), and 93.1 +/- 4.8% of tryptase-positive cells in skin hemangioma (n = 5).
Formalin-fixed specimens of 35 patients with vulvodynia were evaluated immunohistochemically with antibodies to CD 3,4,8,20,117c and human mast cell tryptase, and for WHO-criteria of neoplastic mastocytosis (>25% spindled mast cell, CD25 expression, point mutations of the c-kit gene (D816V), and chronically elevated serum tryptase levels).