Analysis of metabolic syndrome on allergic diseases.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461168
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Respiratory organ internal medicine
• Research Institution: Tokyo National Hospital (Clinical research)
• Principal Investigator: Suzukawa Maho 独立行政法人国立病院機構東京病院(臨床研究部), その他部局等, その他 (20453699)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 喘息 / 肥満 / レプチン / 気道上皮細胞

Outline of Final Research Achievements

The present study investigated the effects of leptin on human airway epithelial cells by using human primary airway epithelial cells and a human airway epithelial cell line, BEAS-2B. Airway epithelial cells expressed leptin receptor (Ob-R). Leptin enhanced ICAM-1 expression and production of CCL11, G-CSF, VEGF, and IL-6 by BEAS-2B cells. Leptin induced migration of primary airway epithelial cells toward leptin, suppressed BEAS-2B apoptosis, and enhanced proliferation of primary airway epithelial cells. In summary, leptin was able to directly activate human airway epithelial cells.

Free Research Field

呼吸器内科