TY - JOUR
T1 - Inhibition of lung microbiota-derived proapoptotic peptides ameliorates acute exacerbation of pulmonary fibrosis
AU - D’Alessandro-Gabazza, Corina N.
AU - Yasuma, Taro
AU - Kobayashi, Tetsu
AU - Toda, Masaaki
AU - Abdel-Hamid, Ahmed M.
AU - Fujimoto, Hajime
AU - Hataji, Osamu
AU - Nakahara, Hiroki
AU - Takeshita, Atsuro
AU - Nishihama, Kota
AU - Okano, Tomohito
AU - Saiki, Haruko
AU - Okano, Yuko
AU - Tomaru, Atsushi
AU - Fridman D’Alessandro, Valeria
AU - Shiraishi, Miyako
AU - Mizoguchi, Akira
AU - Ono, Ryoichi
AU - Ohtsuka, Junpei
AU - Fukumura, Masayuki
AU - Nosaka, Tetsuya
AU - Mi, Xuenan
AU - Shukla, Diwakar
AU - Kataoka, Kensuke
AU - Kondoh, Yasuhiro
AU - Hirose, Masaki
AU - Arai, Toru
AU - Inoue, Yoshikazu
AU - Yano, Yutaka
AU - Mackie, Roderick I.
AU - Cann, Isaac
AU - Gabazza, Esteban C.
N1 - This research was supported in part by the Japan Society for the Promotion of Science (Kakenhi No 17K08442 and 18K08175), in part by a grant from Takeda Science Foundation (2019), Kowa Life Science Foundation (2021), Japan Intractable Diseases (Nanbyo) Research Foundation (2021), GSK Japan Research Grant 2021, and in part by funding support for the Microbiome Metabolic Engineering Theme (Carl R. Woese Institute for Genomic Biology), by the College of Agricultural, Consumer and Environmental Sciences Office of International Programs, the University of Illinois at Urbana-Champaign, and a gift from the Charles and Margaret Levin Family Foundation. The funders had no role in study design, data analysis, decision to publish, or paper preparation.
PY - 2022/12
Y1 - 2022/12
N2 - Idiopathic pulmonary fibrosis is an incurable disease of unknown etiology. Acute exacerbation of idiopathic pulmonary fibrosis is associated with high mortality. Excessive apoptosis of lung epithelial cells occurs in pulmonary fibrosis acute exacerbation. We recently identified corisin, a proapoptotic peptide that triggers acute exacerbation of pulmonary fibrosis. Here, we provide insights into the mechanism underlying the processing and release of corisin. Furthermore, we demonstrate that an anticorisin monoclonal antibody ameliorates lung fibrosis by significantly inhibiting acute exacerbation in the human transforming growth factorβ1 model and acute lung injury in the bleomycin model. By investigating the impact of the anticorisin monoclonal antibody in a general model of acute lung injury, we further unravel the potential of corisin to impact such diseases. These results underscore the role of corisin in the pathogenesis of acute exacerbation of pulmonary fibrosis and acute lung injury and provide a novel approach to treating this incurable disease.
AB - Idiopathic pulmonary fibrosis is an incurable disease of unknown etiology. Acute exacerbation of idiopathic pulmonary fibrosis is associated with high mortality. Excessive apoptosis of lung epithelial cells occurs in pulmonary fibrosis acute exacerbation. We recently identified corisin, a proapoptotic peptide that triggers acute exacerbation of pulmonary fibrosis. Here, we provide insights into the mechanism underlying the processing and release of corisin. Furthermore, we demonstrate that an anticorisin monoclonal antibody ameliorates lung fibrosis by significantly inhibiting acute exacerbation in the human transforming growth factorβ1 model and acute lung injury in the bleomycin model. By investigating the impact of the anticorisin monoclonal antibody in a general model of acute lung injury, we further unravel the potential of corisin to impact such diseases. These results underscore the role of corisin in the pathogenesis of acute exacerbation of pulmonary fibrosis and acute lung injury and provide a novel approach to treating this incurable disease.
UR - http://www.scopus.com/inward/record.url?scp=85126895364&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85126895364&partnerID=8YFLogxK
U2 - 10.1038/s41467-022-29064-3
DO - 10.1038/s41467-022-29064-3
M3 - Article
C2 - 35322016
AN - SCOPUS:85126895364
SN - 2041-1723
VL - 13
JO - Nature communications
JF - Nature communications
IS - 1
M1 - 1558
ER -