The role of S100A8/A9 in the pathogenesis of acute exacerbations of pulmonary fibrosis

American Journal of Physiology-Lung Cellular and Molecular Physiology 2026 Open access

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Authors: Naoki Nakamura, Hisao Higo, Satoru Senoo, Akihiko Taniguchi, Taichi Ozeki, Ryota Sunami, Yumi Inukai, Shusei Yamamoto, Junko Itano, Ayaka Tanaka, Nahoko Tomonobu, Rie Kinoshita
+3 more Masakiyo Sakaguchi, Yoshinobu Maeda, Nobuaki Miyahara
DOI: 10.1152/ajplung.00162.2025
Cited by: 1
References: 55

Abstract

During acute exacerbation of idiopathic interstitial pneumonia, bronchoalveolar lavage fluid (BALF) and serum S100A8/A9 levels were elevated and associated with poor prognosis. In a mouse model of acute pulmonary fibrosis exacerbation, therapeutic targeting of S100A8/A9 attenuated lung inflammation and fibrosis, accompanied by reduced S100A8/A9 levels and neutrophil extracellular traps within airways. In vitro experiments demonstrated that neutrophil-derived S100A8/A9 promoted activation of lung fibroblasts and their differentiation into myofibroblasts, which was effectively inhibited by neutralizing antibodies.

Fields of Study & Subjects

S100 Proteins and Annexins Delphi Technique in Research Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis

Publication details

Journal / source
American Journal of Physiology-Lung Cellular and Molecular Physiology
Publisher
American Physiological Society
Volume
330
Issue
5
Pages
L593–L609
Publication date
11 April 2026
Language
EN