Inhibition of lung microbiota-derived proapoptotic peptides ameliorates acute exacerbation of pulmonary fibrosis

• DOI: 10.1038/s41467-022-29064-3
• Publication Date: 2022-03-23T11:05:57Z
• Authors: Corina N. D’Aless...; Taro Yasuma; Tetsu Kobayashi; Masaaki Toda; Ahmed M. Abdel-Hamid; Hajime Fujimoto; Osamu Hataji; Hiroki Nakahara; Atsuro Takeshita; Kota Nishihama; Tomohito Okano; Haruko Saiki; Yuko Okano; Atsushi Tomaru; Valeria Fridman D...; Miyako Shiraishi; Akira Mizoguchi; Ryoichi Ono; Junpei Ohtsuka; Masayuki Fukumura; Tetsuya Nosaka; Xuenan Mi; Diwakar Shukla; Kensuke Kataoka; Yasuhiro Kondoh; Masaki Hirose; Toru Arai; Yoshikazu Inoue; Yutaka Yano; Roderick I. Mackie; Isaac Cann; Esteban C. Gabazza
• Keywords: Pathogenesis; Diffuse alveolar damage

Abstract Idiopathic pulmonary fibrosis is an incurable disease of unknown etiology. Acute exacerbation idiopathic associated with high mortality. Excessive apoptosis lung epithelial cells occurs in acute exacerbation. We recently identified corisin, a proapoptotic peptide that triggers fibrosis. Here, we provide insights into the mechanism underlying processing and release corisin. Furthermore, demonstrate anticorisin monoclonal antibody ameliorates by significantly inhibiting human transforming growth factorβ1 model injury bleomycin model. By investigating impact general injury, further unravel potential corisin to such diseases. These results underscore role pathogenesis novel approach treating this disease.