Publications by authors named "T Sashio"
Article Synopsis
- Blood eosinophil count is a significant biomarker for managing chronic obstructive pulmonary disease (COPD), but its precise role in the disease still needs further exploration.
- A study with 93 COPD patients showed that 19.3% had eosinophilic COPD, and while eosinophil counts correlated with some blood parameters, they also indicated lung structural changes related to the disease.
- The findings suggest that elevated eosinophils may contribute to alveolar damage and thickening of airway walls in COPD patients lacking asthma, highlighting the need for further research on this inflammation type in COPD.
Background: Sphingosine-1-phosphate (S1P), a lysophospholipid released from inflammatory cells, causes cell migration by increasing cytokines and chemokines. This study was designed to determine whether S1P causes adherence of eosinophils to pulmonary endothelial cells via enhancement of adhesion molecule expression.
Methods: Expression of VCAM-1 and ICAM-1 was assessed by RT-PCR and Western blot analysis in human pulmonary microvasucular endothelial cells (HPMVECs).
What Is Known And Objective: Montelukast, a cysteinyl leukotriene receptor 1 antagonist, is safe and efficacious in patients with asthma. The mechanisms underlying the significant interpatient variability in response to montelukast are not clear but are believed to be, in part, because of genetic variability.
Methods: To examine the associations between polymorphisms in candidate genes in the leukotriene pathway and outcomes in patients with asthma on montelukast for 4-8 weeks, we evaluated the changes in peak expiratory flow (PEF), forced expiratory volume in 1 s (FEV(1·0) ) and patients' subjective symptom before and after montelukast treatment.
Endothelin-1 is considered to be an important mediator in the pathophysiology of asthma because it induces contraction, hypertrophy, and proliferation in airway smooth muscle cells as well as inflammatory responses in the airway. Airway smooth muscle cells have been suggested to contribute to airway inflammation in asthma by producing cytokines. Nevertheless, the role of intracellular Ca(2+) signal in cytokine production in human airway smooth muscle cells is still unclear.
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