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)

To determine the role of hypoxic pulmonary vasoconstriction in pneumococcal pneumonia, hemodynamic measurements were made in 16 dogs before, and within 36 hours after, intrapulmonary administration of type III pneumococcus. Ten dogs with one lobe or more of pneumonia increased their pulmonary vascular resistances and slightly decreased their arterial O2 tensions. Hypoxia increased and hyperoxia decreased their pulmonary vascular resistances. During O2 breathing, arterial PO2 was less during than before the pneumonia and increased when pulmonary perfusion was diverted away from the diseased lung. In 2 dogs breathing air, forcing the cardiac output through the diseased lung caused an increase in vascular resistance that could clearly be reduced by O2 breathing. In 5 dogs, lung mast cell counts showed no decrease in the lobes with pneumonia. In pneumococcal pneumonia, the hypoxic pulmonary pressor mechanism serves to decrease blood flow to the diseased lobes and, thus, to maintain the arterial PO2. Lung mast cells could participate in this response.
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PMID:Preservation of hypoxic pulmonary pressor response in canine pneumococcal pneumonia. 0 Sep 35

In the serum of 43 children the activities of proteinases and peptidases by mean of 41 substrates have been determined in order to get knowledge of overall activities and differentiation of lysosomal proteolytic enzymes. Proteinases, cathepsins A, B, C and D, aminopeptidases, carboxypeptidases, dipeptidases, tripeptidases and aminoacidarylamidases have been checked. The enzyme pattern of the serum of a collective of 15 healthy children or those without serious clinical signs is demonstrated, also the alterations and differentiations in the serum of children with leucemia, pneumonia, inflammatory diseases of the respiratory tract, other inflammatory diseases and common diseases. Leucyl-glycyl-glycyltripeptidase, glycyl-glycyl-glycyltripeptidase, a proteosterase, carboxypeptidase A, a neutrale proteinase and basic proteinase (cathepsin B) and cathepsin C are increased. A distinct elevation has been found only in children with leucemia and pneumonia.
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PMID:[Lysosomal proteinasen and peptidasen in serum of children with inflammatory diseases (author's transl)]. 101 50

The pathogenesis of parainfluenza 1 (Sendai) virus infection was compared among 25-day-old BN, F344, and LEW rats to identify a sensitive as well as a resistant inbred rat strain to Sendai virus-induced lung injury during early life. At 7 days after inoculation, BN rats had 65-fold higher (P less than .001) pulmonary viral titers and threefold higher (P less than .002) numbers of neutrophils in bronchoalveolar lavage fluid than did F344 rats. At 14 days after inoculation, when most virus-induced inflammation had been resolved, BN rats had a threefold greater (P less than .01) incidence of bronchioles with aggregates of lymphocytes and macrophages than did F344 rats. Control BN rats had higher numbers of bronchiolar eosinophils than did F344 or LEW rats. Although viral inoculation resulted in increased numbers of bronchiolar mast cells in all three strains at 14 days, bronchiolar mast cell density was greater (P less than .005) in virus-inoculated BN and LEW rats than in F344 rats. We conclude that BN rats are high responders and F344 rats are low responders to Sendai virus-induced bronchiolitis, pneumonia, and airway mastocytosis. These strain differences may be useful in elucidating important pathogenetic mechanisms in virus-induced airway injury and mastocytosis.
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PMID:Brown Norway rats are high responders to bronchiolitis, pneumonia, and bronchiolar mastocytosis induced by parainfluenza virus. 166 31

Current concepts regarding the morphology, constituents, distribution, and kinetics of the eosinophil allow an expanded understanding of the eosinophil's function in health and disease. In particular, certain eosinophil constituents may have beneficial effects (modulation of mast cell-dependent reactions and helminthotoxic properties), while others may produce detrimental effects (tissue destruction). Eosinophils may be clinically important in obstructive and infiltrative pulmonary diseases. In obstructive disease, a peripheral eosinophilia indicates reversibility, and the magnitude of the peripheral eosinophil count correlates with the severity of the reversible obstruction. Concerning infiltrative pulmonary disease, an updated classification of pulmonary infiltrates with eosinophilia, which is based on recognizable causes and syndromes, is presented, and allergic bronchopulmonary aspergillosis, chronic eosinophilic pneumonia, drug reactions, the hypereosinophilic syndrome, parasitic infestations, and the Churg-Strauss syndrome are specifically considered.
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PMID:The eosinophil and the lung. 710 33

Fibrotic lung disorders are chronic inflammatory diseases in which inflammatory processes in the lower respiratory tract injure the lung and modulate the proliferation of mesenchymal cells that form the basis of the fibrotic scar. The pathogenesis of fibrosis in fibrotic lung disorders remains unclear; however, recent attention has focused on the potential role of the mast cell in the genesis of fibrosis. To determine whether mast cells are implicated in the pathogenesis of lung fibrosis, mast cells were compared with the degree of fibrosis in transbronchial lung biopsy specimens from 49 patients with fibrotic lung disorders (16 sarcoidosis, 15 farmer's lung disease, 9 cryptogenic fibrosing alveolitis, 6 bronchiolitis obliterans organizing pneumonia, 3 histiocytosis X). In lung tissue of patients with fibrotic lung disorders, there was an increased number of mast cells in respect to the control group (98.6 +/- 7.7 vs 27.8 +/- 5.1 mast cells per square millimeter, p < 0.01). Mast cell counts in lung biopsy specimens were significantly correlated with the degree of fibrosis (r = 0.87, p < 0.001); 80.8 percent of mast cells were found in the alveolar septa, 9.6 percent within alveoli, 1.9 percent among alveolar lining cells, and 5 percent along blood vessels. No mast cells were located within alveoli in controls. Our data suggest that mast cells participate in chronic inflammation and that their presence is related to interstitial fibrosis in a much broader spectrum of fibrotic lung disorders.
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PMID:Mast cells in fibrotic lung disorders. 813 13

The detailed mechanisms which can explain the inherent radiosensitivity of salivary glands remain to be elucidated. Although DNA is the most plausible critical target for the lethal effects of irradiation, interactions with other constituents, such as cell membrane and neuropeptides, have been suggested to cause important physiological changes. Moreover, mast cells seem to be closely linked to radiation-induced pneumonitis. Therefore, in the present study the effects of fractionated irradiation on salivary glands have been assessed with special regard to the appearance of mast cells and its correlation with damage to gland parenchyma. Sprague-Dawley strain rats were unilaterally irradiated to the head and neck with the salivary glands within the radiation field. The irradiation was delivered once daily for 5 days to a total dose of 20, 35 and 45 Gy. The contralateral parotid and submandibular glands served as intra-animal controls and parallel analysis of glands was performed 2, 4, 10 or 180 days following the last radiation treatment. Morphological analysis revealed no obvious changes up to 10 days after the irradiation. At 180 days a radiation dose-dependent loss of gland parenchyma was seen, especially with regard to serious acinar cells in parotid gland and acinar cells and serous CGT (convoluted granular tubule) cells in the submandibular gland. These changes displayed a close correlation with a concomitant dose-dependent enhanced density of mast cells and staining for hyaluronic acid. This cell population seems to conform with the features of the connective tissue mast cell type. The parotid seems to be more sensitive to irradiation than the submandibular gland. Thus, the present results further strengthen the role of and the potential interaction of mast cells with radiation-induced tissue injury and alterations in normal tissue integrity.
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PMID:Increase in mast cells and hyaluronic acid correlates to radiation-induced damage and loss of serous acinar cells in salivary glands: the parotid and submandibular glands differ in radiation sensitivity. 829 28

A role of eosinophil is thought to be an inflammatory effect, although it had been believed that the cell has a protective role by blocking mediators from the mast cell. Eosinophils release several kinds of basic and cationic proteins following receptor-mediated activation. These mediators gradually lead to tissue damage of the bronchi, skin, nerve, heart and other general organs. Bronchial asthma and eosinophilic pneumonia as well as hyper-eosinophilic syndrome is based on this pathogenesis. Potent therapy, including steroids, will be needed for long terms in these diseases with tissue eosinophilia.
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PMID:[Inflammatory role of eosinophil in allergic reactions]. 849 39

Idiopathic bronchiolitis obliterans organizing pneumonia (BOOP) is characterized by air space inflammation and fibrosis of unknown origin. The pathogenesis of the inflammatory reaction and fibrosis in fibrotic lung disorders remains unclear; however, recent attention has focused on the potential role of the mast cell in the genesis of fibrosis. To determine whether mast cells are implicated in the pathogenesis of BOOP, mast cells were identified in BAL fluid and in transbronchial lung biopsy specimens from 11 patients affected by BOOP and 17 control subjects. Mast cells and tryptase were significantly increased in BAL fluid of patients with BOOP (p = 0.001 and p = 0.03, respectively). In lung tissue of patients with BOOP, there was an increased number of mast cells per square millimeter of lung tissue with respect to control group (p = 0.001). Seventy-three percent of mast cells were found in the alveolar septa, 18% within alveoli often plunged in organizing pneumonia, 4% among alveolar lining cells, and 6% along blood vessels. No mast cells were located within alveoli in control subjects. Mast cell degranulation was evident in lung tissue specimens of patients with BOOP but not in those of control subjects (p = 0.01). This study shows the importance of mast cells and mast cell activation in the pathogenesis of BOOP.
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PMID:Mast cells in bronchiolitis obliterans organizing pneumonia. Mast cell hyperplasia and evidence for extracellular release of tryptase. 869 38

The predominant pathogen in patients with cystic fibrosis (CF) is Pseudomonas aeruginosa, which results in a chronic lung infection associated with progressive pulmonary insufficiency. In a rat model of chronic P. aeruginosa pneumonia mimicking that in patients with CF, we studied whether the inflammation and antibody responses could be changed by treatment with the Chinese herbal medicine ginseng. An aqueous extract of ginseng was injected subcutaneously, and cortisone and saline were used as controls. Two weeks after challenge with P. aeruginosa, the ginseng-treated group showed a significantly improved bacterial clearance from the lungs (P < 0.04), less severe lung pathology (P = 0.05), lower lung abscess incidence (P < 0.01), and fewer mast cell numbers in the lung foci (P < 0.005). Furthermore, lower total immunoglobulin G (IgG) levels (P < 0.01) and higher IgG2a levels (P < 0.025) in serum against P. aeruginosa sonicate and a shift from an acute type to a chronic type of lung inflammation compared to those in the control and cortisone-treated groups were observed. These findings indicate that ginseng treatment of an experimental P. aeruginosa pneumonia in rats promotes a cellular response resembling a TH1-like response. On the basis of these results it is suggested that ginseng may have the potential to be a promising natural medicine, in conjunction with other forms of treatment, for CF patients with chronic P. aeruginosa lung infection.
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PMID:Ginseng treatment reduces bacterial load and lung pathology in chronic Pseudomonas aeruginosa pneumonia in rats. 914 52

Variations in the host response during pneumonia caused by Streptococcus pneumoniae in susceptible (CBA/Ca) and resistant (BALB/c) inbred mouse strains were investigated. Significant differences were detected in survival time, core body temperature, lung-associated and systemic bacterial loads, mast cell numbers, magnitude and location of cytokine production, lung disruption, and ability of isolated lung cells to release the cytokine tumor necrosis factor (TNF) alpha in vitro. Overall, the results indicate that the reduced capacity of CBA/Ca mice to induce rapid TNF activity within the airways following infection with S. pneumoniae may be a factor in their elevated susceptibility to pneumococcal pneumonia.
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PMID:Role of inflammatory mediators in resistance and susceptibility to pneumococcal infection. 1185 43


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