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Biomedical subjects

Mutsuo Yamaya

Publications and source records attributed to Mutsuo Yamaya.

49 records · Page 3Linked to original sources
PubMed2003

Transient relief of asthma symptoms during jaundice: a possible beneficial role of bilirubin.

Bilirubin arises from enzymatic reduction by biliverdin reductase of biliverdin, a product of heme oxygenase activity. Recent literature describes that bilirubin is a major physiologic antioxidant that can protect cells from chemical oxidants such as hydrogen peroxide. Recently, it has been reported that oxidative stress may play a crucial role in the pathogenesis of asthma. We report a case of complete resolution of persistent difficult-to-control asthma in accordance with increased levels of serum bilirubin due to acute hepatitis B. The present case suggests that anti-oxidative agents might be effective for the treatment of asthma.

Adolescent↗
PubMed2003

[Cerebrovascular disease and pneumonia in the elderly].

Pneumonia is a common cause of death in elderly people. A series of our studies have demonstrated that pneumonia in the elderly is characterized by silent aspiration, impaired swallowing and cough reflex, partly due to cerebral infarctions at basal ganglia. These infarctions probably induce the disruption of the specific central neurotransmitter system including dopamine and substance P, which plays an important role for swallowing and cough reflex. Use of ACE inhibitor and stimulation of the oral cavity by simple oral care, which are effective in increasing substance P. reduced the incidence of aspiration pneumonia. Moreover, use of a dopamine agonist such as amantadine hydrochloride and a folic acid supplement that are known to potentiate dopaminergic neurons also prevented aspiration pneumonia. For patients bedridden due to lowered ADL, it is essential for them to keep an upright position a few hours after meals to prevent aspiration pneumonia caused by the reflux of ingested foods. Also, administration of neuroleptics may cause aspiration pneumonia by suppression of dopaminergic neurons.

Activities of Daily Living↗
PubMed2002

Effects of rhinovirus infection on histamine and cytokine production by cell lines from human mast cells and basophils.

To understand the biochemical events that occur in the airways after rhinovirus (RV) infection, we developed for the first time a model in which the cell lines from human mast cells (HMC-1) and basophils (KU812) can be infected with RV14, a major group RV. Viral infection was confirmed by demonstrating that viral titers in culture supernatants, and RV RNA increased with time. RV14 infection alone and a combination of PMA plus calcium ionophore A23187, did not increase histamine production by these cells, although IgE plus anti-IgE increased the histamine production. However, histamine content in the supernatants increased in response to PMA plus A23187, or IgE plus anti-IgE after RV14 infection. PMA plus A23187 or IgE plus anti-IgE induced the production of IL-8 and GM-CSF in supernatants of HMC-1 cells and IL-4 and IL-6 in supernatants of KU812 cells. RV14 infection further increased the production of the cytokines, whereas RV14 infection alone did not alter the production of the cytokines by these cells. An Ab to ICAM-1 inhibited RV14 infection of the cells and decreased the production of cytokines and histamine after RV14 infection. RV14 infection enhanced the increases in intracellular calcium concentration and activation of NF-kappaB by PMA plus A23187 in the cells. These findings suggest that RV14 infection may prime the cytokine and histamine production from mast cells and basophils and may cause airway inflammation in asthma.

Basophils↗
PubMed2002

Erythromycin inhibits rhinovirus infection in cultured human tracheal epithelial cells.

To examine the effects of erythromycin on rhinovirus (RV) infection in airway epithelium, primary cultures of human tracheal epithelial cells were infected with the RV major subgroup, RV14, and the minor subgroup, RV2. Infection was confirmed by increases in viral RNA of the infected cells and viral titers of the supernatants. RV14 upregulated the expression of the mRNA and protein of intercellular adhesion molecule-1 (ICAM-1), the major RV receptor, and it increased the cytokine production. Erythromycin reduced the supernatant RV14 titers, RV14 RNA, the susceptibility to RV14 infection, and the production of ICAM-1 and cytokines. Erythromycin also reduced the supernatant RV2 titers, RV2 RNA, the susceptibility to RV2 infection, and cytokine production, although the inhibitory effects of erythromycin on the expression of the low-density lipoprotein receptor, the minor RV receptor, were small. Erythromycin reduced the nuclear factor-kappaB activation by RV14 and decreased the number of acidic endosomes in the epithelial cells. These results suggest that erythromycin inhibits infection by the major RV subgroup by reducing ICAM-1 and infection by both RV subgroups by blocking the RV RNA entry into the endosomes. Erythromycin may also modulate airway inflammation by reducing the production of proinflammatory cytokines and ICAM-1 induced by RV infection.

Anti-Bacterial Agents↗
PubMed2002

Bilirubin ameliorates bleomycin-induced pulmonary fibrosis in rats.

Many possible treatments for pulmonary fibrosis have been investigated, but except for some current clinical trials, none have succeeded in clinical trials. On the basis of the antioxidant action of bilirubin (BIL), we examined the effects of hyperbilirubinemia on the development of bleomycin (BLM)-induced pulmonary fibrosis in rats. The animals' plasma BIL level was kept within 3 and 10 mg/dl by repeated intravenous infusion of a high dose of BIL. We studied the inhibitory effects of hyperbilirubinemia on BLM-induced pulmonary fibrosis through histopathologic and biochemical analyses. Mortality of rats with BLM-induced pulmonary fibrosis was significantly lower in the three groups with hyperbilirubinemia. The ameliorating effect of hyperbilirubinemia on pulmonary fibrosis was shown by lung histology, as well as by a decreased lung content of hydroxyproline and reduced bronchoalveolar lavage fluid (BALF) concentration of transforming growth factor (TGF)-beta(1). The number of polymorphonuclear leukocytes and lymphocytes in BALF was also decreased in the groups with hyperbilirubinemia. Furthermore, oxidative metabolites of BIL in urine were present at significantly higher levels in BLM-treated rats with hyperbilirubinemia than in those without hyperbilirubinemia. These data suggest that the antioxidative action of BIL can attenuate BLM-induced pulmonary fibrosis, partly by inhibiting lung inflammation and production of TGF-beta1.

Animals↗
PubMed2002

Acid stimulation reduces bactericidal activity of surface liquid in cultured human airway epithelial cells.

To examine the effects of acid exposure with moderate acidity (pH 3.0-5.0) on bactericidal activity of airway surface liquid (ASL), ASL was collected by washing the surface of primary cultures of human tracheal epithelial cells 24 h after treatment with phosphate-buffered saline (PBS) adjusted to a pH of 3.0, 4.0, or 5.0. In all ASL, bactericidal activity was sensitive to sodium concentration. Escherichia coli (500 colony forming units [CFU]) was incubated in ASL, and the number of surviving bacteria was examined. The number of surviving bacteria in ASL from cultured cells with acid exposure at pH 3.0-5.0 was significantly higher than that in control ASL. The minimum inhibitory dilution ratio of ASL against 500 CFU of E. coli was also examined by microdilution assays. According to this assay, the bactericidal activity in ASL with acid challenge at a pH of 3.0 was less than half of that in control ASL. Reverse transcription-polymerase chain reaction and Western blot analysis showed that the production of mRNA and protein of human beta-defensin (HBD)-1 were significantly decreased by acid exposure at pH 3.0-5.0. In contrast, acid exposure did not change the production of mRNA and protein of HBD-2 and beta-actin mRNA. These results indicate that acid exposure, even with moderate acidity, may inhibit the production of bactericidal molecules, including HBD-1, in airway epithelial cells. Acid exposure may reduce bactericidal activity of ASL in human airway epithelial cells and may increase susceptibility of the airway to bacterial infection.

Actins↗
PubMed2002

[Etiology, pathogenesis and management of senile inflammatory pulmonary diseases].

We studied the etiology, pathogenesis and management of therapy-resistant inflammatory pulmonary diseases. First, to understand the pathogenesis of rhinovirus (RV) infection-induced exacerbation of bronchial asthma, we infected cultured human tracheal epithelial cells with RV. The epithelial cells produced a variety of proinflammatory cytokines, intercellular adhesion molecules (ICAM-1) and low-density lipoprotein receptor, and increased the permeability across the epithelial cells. These findings suggest that these factors and the increased permeability may cause airway inflammation, resulting in the exacerbation of asthma. Glucocorticoid and bafilomycin inhibited RV infection in the epithelial cells by reducing ICAM-1 expression and RV RNA entry from the acidic endosomes to the cytoplasm. Second, we revealed the mechanisms of aspiration pneumonia induced by silent aspiration in patients with cerebral infarction. We also developed a pharmacologic treatment for preventing aspiration pneumonia with amantadine, which stimulates the dopaminergic neurons; the angiotensin-converting enzyme inhibitors, which decrease substance P catabolism; and cilostazol, which inhibits platelet aggregation and induces cerebral vasodilation. Third, we demonstrated that exhaled carbon monoxide concentrations caused by heme oxygenase-1 upregulation, may be a useful noninvasive means of monitoring airway inflammation and of controlling elderly patients with bronchial asthma. Finally, we demonstrated that microsatellite polymorphism in the heme oxygenase-1 gene promoter is associated with susceptibility to emphysema caused by cigarette smoke in Japanese patients with chronic pulmonary emphysema.

Aged↗
PubMed2002

[Criteria of impairment of pulmonary function using Japanese standard values].

According to the law of functional impairment, cases of impairment of pulmonary function are designated as 1st, 3rd and 4th grade impairment. The criteria of pulmonary function a based on Baldwin's predicted values. Recently, the Japanese Respiratory Society reported the Japanese standard values for pulmonary function. In the present study, we compared the numbers of patients classified into the three grades using the Japanese values and Baldwin's values. We found that from about 10 to 20 percent of patients appeared in a higher grade when Japanese standard values were used instead of Baldwin's values. We suggest that Japanese standard values should be used in order to judge the impairment of these patients.

Aged↗