A5103066313- Asthma and respiratory diseases
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Pediatric health and respiratory diseases
- Air Quality and Health Impacts
- Respiratory and Cough-Related Research
- Tracheal and airway disorders
- Neonatal Respiratory Health Research
- Pneumonia and Respiratory Infections
- Energy and Environment Impacts
- Medical Imaging and Pathology Studies
- IL-33, ST2, and ILC Pathways
- Pleural and Pulmonary Diseases
- Respiratory Support and Mechanisms
- Respiratory viral infections research
- Inhalation and Respiratory Drug Delivery
- Indoor Air Quality and Microbial Exposure
- Immune Response and Inflammation
- Lung Cancer Diagnosis and Treatment
- Noise Effects and Management
- Sarcoidosis and Beryllium Toxicity Research
- Antifungal resistance and susceptibility
- Immune Cell Function and Interaction
- Eosinophilic Disorders and Syndromes
- Lung Cancer Treatments and Mutations
Kyorin University
2014-2023
Kyorin University Hospital
2012-2016
The University of Tokyo
1999-2014
Teikyo University
2000-2011
Respiratory Clinical Trials
2004
University of Nebraska Medical Center
1990-2002
GlaxoSmithKline (Japan)
2002
Mount Sinai Hospital
2002
Kanazawa University
2002
Osaka University
2002
Tobacco smoke is believed to cause small airway disease and then chronic obstructive pulmonary (COPD), but the molecular mechanisms by which obstruction occurs remain unknown. To study gene expression levels of transforming growth factor (TGF)-beta1, a potent fibrogenic factor, in epithelium from smokers patients with COPD, we harvested highly pure samples epithelial cells airways under direct vision using an ultrathin bronchofiberscope BF-2.7T (outer diameter 2.7 mm biopsy channel 0.8...
Abstract Thymus- and activation-regulated chemokine (TARC; CCL17) is a lymphocyte-directed CC that specifically chemoattracts receptor 4-positive (CCR4+) Th2 cells. To establish the pathophysiological roles of TARC in vivo, we investigated here whether an mAb against could inhibit induction asthmatic reaction mice elicited by OVA. was constitutively expressed lung up-regulated allergic inflammation. The specific Ab attenuated OVA-induced airway eosinophilia diminished degree...
Erythromycin (EM) and its 14-member macrolide analogues have attracted attention for effectiveness in a variety of airway diseases, including diffuse panbronchiolitis (DPB), sinobronchial syndrome, chronic sinusitis. However, mechanisms action remain unelucidated. We evaluated the effects several antibiotics on IL-8 expression by normal transformed human bronchial epithelial cells, an important source this potent chemokine involved cell recruitment into airways. EM clarithromycin (CAM)...
Asthma is characterized by chronic inflammation of the airway with presence Th2 cytokines. Airway remodeling in asthma closely related to clinical manifestations. Lung myofibroblasts play a critical role and cytokines may modulate their behavior. We examined effect two major cytokines, IL-4 IL-13, on differentiation lung fibroblasts myofibroblasts. hypothesized that these would stimulate fibroblast proliferation association decreased prostaglandin E(2) (PGE(2)).Lung were incubated IL-13 or...
Air pollutants including diesel exhaust particles (DEPs) have been shown to enhance allergic responses. DEPs stimulate airway epithelial cells produce various cytokines; however, the intracellular signal transduction pathway and involvement of reduction oxidation (redox) control in DEP-activated signaling not determined. In present study, we therefore examined role p38 mitogen-activated protein (MAP) kinase DEP-induced interleukin 8 (IL-8) RANTES production by human bronchial (BECs) order...
Abstract Fine particles derived from diesel engines (diesel exhaust particles, DEP) have attracted attention, since their density in industrial countries seems related to the increased prevalence of pulmonary diseases. Previous studies suggested that DEP a potential directly activate airway epithelial cells produce and release inflammatory cytokines mediators, thus facilitate responses lung. To elucidate molecular mechanisms action, we studied here IL-8 gene expression, one important...
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Vascular endothelial growth factor (VEGF)/vascular permeability induces both angiogenesis and vascular mainly through VEGF receptor (VEGFR)-2 activation. binds VEGFR-1 as well, but the importance of signaling in has been largely neglected. Here, we report purification characterization a novel VEGF-like protein from Trimeresurus flavoviridis Habu snake venom. The venom-specific molecule, T. venom (TfsvVEGF), addition to VEGF-A. TfsvVEGF almost 10-fold less mitotic activity than VEGF(165),...
Long-term macrolide therapy has been proven to improve survival in patients with diffuse panbronchiolitis. Although its mechanisms remain unknown, previous studies have suggested the effects of might be anti-inflammatory rather than antibacterial. To elucidate molecular action, we studied here erythromycin (EM) and new derivative, EM703, which shows no antibacterial on activation transcription factor nuclear factor-kappaB (NF-kappaB) human bronchial epithelial cells. Western blotting...
<i>Background:</i> Airway remodeling is an important feature of chronic airway disease, but the mechanisms involved remain unclear. Recently, epithelial mesenchymal transition (EMT) was reported to be associated with tissue fibrosis. TGF-β1, which a potent inducer EMT, thought related pathogenesis remodeling. We investigated whether TGF-β1 and/or TNF-α induce EMT in bronchial cells. <i>Methods:</i> Cultured BEAS-2B cells and primary normal human (NHBE) were treated...
Recently, epithelial-mesenchymal transition (EMT) has been reported to contribute tissue fibrosis through enhanced transforming growth factor (TGF)-β1 signaling. Tumor necrosis (TNF)-α also implicated in fibrosis. Therefore, the authors investigated whether TNF-α affected TGF-β1–induced EMT. Cultured alveolar epithelial cells (A549 cells) were stimulated with TGF-β1 (5 ng/mL), with/without (10 ng/mL). induced EMT of A549 cells, loss E-cadherin and acquisition vimentin. Combination EMT,...
Background A randomised controlled trial in Japan showed that inhaled N-acetylcysteine monotherapy stabilised serial decline forced vital capacity (FVC) some patients with early idiopathic pulmonary fibrosis (IPF). However, the efficacy and tolerability of combination therapy an antifibrotic agent are unknown. Methods This 48-week, randomised, open-label, multicentre phase 3 compared pirfenidone plus 352.4 mg twice daily results for alone IPF. The primary end-point was annual rate FVC....
We evaluated the effect of roxithromycin on cytokine production and neutrophil attachment to human airway epithelial cells. Roxithromycin suppressed interleukin 8 (IL-8), IL-6, granulocyte-macrophage colony-stimulating factor. It inhibited adhesion modulates local recruitment activation inflammatory cells, which may have relevance its efficacy in diseases.
Section:ChooseTop of pageAbstract <<Materials and MethodsResultsDiscussionReferencesCITING ARTICLES
Therapies that mitigate the fibrotic process may be able to slow progressive loss of function in many lung diseases. Because cyclic adenosine monophosphate is known regulate fibroblasts, current study was designed evaluate activity selective phosphodiesterase (PDE) inhibitors on two vitro fibroblast responses: chemotaxis and contraction three-dimensional collagen gels. Selective PDE4 inhibitors, rolipram cilomilast, each inhibited human fetal fibroblasts (HFL-1) toward fibronectin blindwell...
To study the inflammatory responses of small-airway epithelium in smokers, we harvested enough living epithelial cells (1.97 × 10 6 ± 0.74 ) with a new ultrathin fiberscope from very peripheral airways 22 current smokers and 17 subjects who never smoked after informed consent was obtained. The were keratin positive composed mainly nonciliated cells. expression levels markers [interleukin (IL)-8 intercellular adhesion molecule (ICAM)-1] evaluated RT-PCR. magnitude mRNA corrected by β-actin...
Endothelin is a potent bronchoconstrictor peptide first identified as novel vasoconstrictor produced by vascular endothelial cells. Recent reports suggest that airway epithelial cells are also capable of releasing this active peptide. To investigate the regulatory mechanism endothelin expression, we studied effects endotoxin and pro-inflammatory cytokines such interleukin-1 tumour necrosis factor on expression release endothelin-1 Both stimulated human bronchial Northern blot analysis showed...