The role of auto-immune antibody for collagen type V with gastroesphageal reflux disease for the pathogenesis of idiopathic pulmonary fibrosis

• Project/Area Number: 25860636
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Respiratory organ internal medicine
• Research Institution: Chiba Cancer Center (Research Institute) (2016); Chiba University (2013-2015)
• Principal Investigator: Takekazu Iwata 千葉県がんセンター(研究所), 呼吸器外科, 主任医長 (30586681)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Project Status: Completed (Fiscal Year 2016)
• Budget Amount: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000); Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000); Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000); Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
• Keywords: 特発性肺線維症 / 逆流性食道炎 / GERD / ピルフェニドン

Outline of Final Research Achievements

The aim of this study is to investigate the correlation of idiopathic pulmonary fibrosis(IPF) and auto-immune antibody for collagen type V (col(V)) with gastroesphageal reflux disease(GERD). We hypothesized that IPF was correlated to the auto-immune antibody for col(V) driven by lung stromal tissue damage and remodeling caused by GERD.
The analysis of the patients who undertaken lung cancer surgery in our institution revealed that the IPF patients have four times more GERD than non-IPF patients（Fisher exact test p=0.013). The col(V) and IL17A does not overexpressed in the lung of IPF in mRNA expression levels. The DNA microarray analysis proven TNF signaling pathway in cluding CXCL1, CXCL2, CXCL3 in IPF with GERD specifically.