Abstract Background: Asthma is a heterogeneous syndrome substantiating the urgent requirement for endotype-specific biomarkers. Dysbalance of fibrosis and fibrolysis in asthmatic lung tissue leads to reduced levels of the inflammation-protective collagen 4 (COL4A3). Objective: To delineate the degradation of COL4A3 in allergic airway inflammation and evaluate the resultant product as a biomarker for anti-IgE therapy response. Methods: The serological COL4A3 degradation marker C4Ma3 (Nordic Bioscience, Denmark) and serum cytokines were measured in the ALLIANCE cohort (pediatric cases/controls: 134/35; adult cases/controls: 149/31). Exacerbation of allergic airway disease in mice was induced by sensitising to OVA, challenge with OVA aerosol and instillation of poly(cytidylic-inosinic). Fulacimstat (chymase inhibitor, Bayer) was used to determine the role of mast cell chymase in COL4A3 degradation. Patients with cystic fibrosis (CF,
July 29, 2021
Eur Respir J
Weckmann M, Bahmer T, Rønnow S, Pech M, Vermeulen C, Faiz A, Karsdal MA, Lunding L, Oliver B, Wegmann M, Ulrich-Merzenich G, Juergens U, Duhn J, Laumonnier Y, Danov O, Sewald K, Zissler U, Jonker M, König I, Hansen G, Mutius E, Fuchs O, Dittrich AM, Schaub B, Happle C, Rabe K, de Berge M, Burgess J, Kopp M, Leeming DJ, Bülow Sand JM
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