ArticleInternational archives of allergy and immunology2025
Phospho-Proteomic Analysis of Interleukin-13 Signaling in Airway Cells Reveals SRC Family Kinase Involvement in Interleukin-13-Induced Inflammatory Responses.
Article in International archives of allergy and immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionAllergic asthma is a chronic inflammatory airway disease driven by the cytokine interleukin-13 (IL-13). Although IL-13 signals through the canonical JAK1/TYK2/STAT6 pathway, our understanding of the totality of IL-13-induced signaling intermediates is incomplete.
methodsTo address this, we performed a phospho-proteomic analysis of IL-13-stimulated A549 human airway epithelial cells. IL-13 stimulation led to differential phosphorylation at 145 unique serine/threonine residues across 92 proteins involved in diverse cellular processes. In silico analysis was used to predict kinases responsible for the observed changes, and therapeutics which may reduce IL-13-mediated pathology. The activation of these kinases and the ability of these therapeutics to limit IL-13 activity were tested in vitro using molecular techniques and in vivo in an IL-13-induced model of asthma.
resultsAnalysis of IL-13-induced differentially phosphorylated proteins revealed activation of several pathways including RNA splicing, cytoskeletal remodeling, GTPase activity, and focal adhesion complex formation. Network analysis identified SRC family kinases (SFKs), a family of non-receptor tyrosine kinases, as potential regulators of IL-13-induced changes in phosphorylation, and dasatinib, a pan-SFK inhibitor, as a potential inhibitor of IL-13 signaling. In both human and mouse lung fibroblasts, molecular approaches demonstrated activation of SFKs following IL-13 stimulation. In vitro, dasatinib reduced IL-13-induced STAT6 phosphorylation and downstream gene expression. In vivo, dasatinib attenuated IL-13-induced airway hyperresponsiveness without significantly affecting inflammatory cell infiltration or gene expression in bronchoalveolar lavage fluid.
conclusionThese findings support a potential therapeutic role for dasatinib in inhibition of IL-13-driven responses such as those observed in allergic asthma.
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