A5036911946- Asthma and respiratory diseases
- Chronic Obstructive Pulmonary Disease (COPD) Research
- IL-33, ST2, and ILC Pathways
- Glycosylation and Glycoproteins Research
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Pediatric health and respiratory diseases
- Neonatal Respiratory Health Research
- Pulmonary Hypertension Research and Treatments
- Genomics, phytochemicals, and oxidative stress
- Mycobacterium research and diagnosis
- Proteoglycans and glycosaminoglycans research
- Immune Cell Function and Interaction
- Galectins and Cancer Biology
- Lung Cancer Research Studies
- Medical and Health Sciences Research
- Carbohydrate Chemistry and Synthesis
- Inhalation and Respiratory Drug Delivery
- Antifungal resistance and susceptibility
- Protease and Inhibitor Mechanisms
- Tracheal and airway disorders
- Air Quality and Health Impacts
- Cancer Immunotherapy and Biomarkers
- Lung Cancer Treatments and Mutations
- Neuroendocrine Tumor Research Advances
- Cytokine Signaling Pathways and Interactions
University of Tsukuba
2007-2024
Tsukuba Memorial Hospital
2019
Johns Hopkins University
2011-2018
Johns Hopkins Medicine
2012-2015
University of Georgia
2012
Ibarakihigashi National Hospital
2010
National Hospital Organization
2010
Nagoya University
2005
National Hospital Organization Mito Medical Center
2004
Inflammation, protease/anti‐protease imbalance and oxidative stress play important roles in the pathogenesis of emphysema. Nrf2 counteracts tissue damage inflammation through transcriptional activation via anti‐oxidant responsive element (ARE). To clarify protective role development emphysema, susceptibility Nrf2‐knockout mice to cigarette smoke (CS)‐induced emphysema was examined. In ‐knockout mice, first observed at 8 weeks exacerbated by 16 following CS‐exposure, whereas no pathological...
Abstract Emphysema is one of the major pathological abnormalities associated with chronic obstructive pulmonary disease. The protease/antiprotease imbalance and inflammation resulting from oxidative stress have been attributed to pathogenesis emphysema. Nrf2 believed protect against tissue damage through transcriptional activation a battery antioxidant enzymes. In this study, we investigated protective role in development emphysema using elastase-induced as our model system. We found that...
Acute lung injury (ALI) is a disease process that characterized by diffuse inflammation in the parenchyma. Recent studies demonstrated cyclooxygenase-2 (COX-2) induced at late phase of aids resolution generating 15-deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2). Transcription factor Nrf2 activated electrophiles and exerts antiinflammatory effects inducing gene expression antioxidant detoxification enzymes.Because 15d-PGJ2 an endogenous electrophile, we hypothesized it protects against ALI...
Airway remodeling is an important feature of chronic asthma that causes irreversible airflow obstruction. Although considered to be a Th2 disease, the role T-bet and GATA-3, key transcription factors for differentiation toward Th1 cells, in pathogenesis airway poorly understood.We therefore examined effects GATA-3 or induction Th1/Th2 bias on development mice.The after repeated allergen challenges was analyzed using transgenic mice overexpressing either T-bet.The degrees subepithelial...
Asthma is a heterogeneous disease that can be broadly classified into type 2, which primarily steroid-sensitive and eosinophilic, non-type steroid-resistant neutrophilic. While the mechanisms leading to development of molecular-targeted therapies for 2 asthma are being elucidated, much remains learned about asthma. To investigate role oxidative stress in refractory allergic airway inflammation, we compared models generated by immunizing wild-type nuclear factor erythroid-2-related...
To clarify the essential role of NKT cells in allergy, we investigated contribution to pathogenesis eosinophilic airway inflammation using alpha-galactosylceramide (alpha-GalCer), a selective ligand for cells. Although continuous administration alpha-GalCer during ovalbumin (OVA) sensitization increased OVA-specific IgE levels and worsened eosinophil inflammation, single at time OVA challenge completely prevented infiltration wild-type mice. This inhibitory effect was associated with...
Nontuberculous mycobacteria (NTM) are an important cause of morbidity and mortality in pulmonary infections. Among them, Mycobacterium avium complex (MAC) is the most common NTM disease worldwide.
Rationale: Hypersensitivity pneumonitis (HP) is mediated by a Th1 immune response. Transcription factor GATA binding protein-3 (GATA-3) believed to be key regulator of Th2 differentiation and thus might play regulatory roles in the pathogenesis hypersensitivity (HP).Objectives: We examined effect GATA-3 overexpression on development HP mice.Methods: Wild-type C57BL/6 mice GATA-3–overexpressing same background were used this study. was induced repeated exposure Saccharopolyspora rectivirgula,...
Activation of the cyclic AMP (cAMP) signaling pathway leads to suppression inflammation in airways and relaxation airway smooth muscle. Intracellular cAMP levels are determined by a balance between activities adenylate cyclase phosphodiesterases. We hypothesized that polymorphisms phosphodiesterase 4D (PDE4D) gene activate its protein function which downregulation cAMP, resulting development chronic obstructive pulmonary disease (COPD). A case-control study was performed using Japanese (96...
Siglec-F is a pro-apoptotic receptor on mouse eosinophils that recognizes 6'-sulfated sialyl Lewis X and N-acetyl-lactosamine as well multivalent structures glycan arrays. We hypothesized attenuation of the carbohydrate sulfotransferase 1 (CHST1) gene encoding keratan sulfate galactose 6-O-sulfotransferase, an enzyme likely required for 6'-sulfation some these putative ligands, would result in decreased lung ligand levels enhanced allergic eosinophilic airway inflammation. Tissue analysis...
Background We demonstrated previously that GATA-3 overexpression markedly enhanced allergen-induced airway inflammation and remodelling, including subepithelial fibrosis, smooth muscle cell hyperplasia, in transgenic mice. Objective Because cysteinyl leukotrienes (cysLTs) have been shown to be involved such structural changes, the effects of a specific cysLT1 receptor antagonist, montelukast, were evaluated mouse model chronic asthma. Methods GATA-3-overexpressing mice wild-type Balb/c...