ArticleAnimal models and experimental medicine2026
Establishment of a mouse model of propylthiouracil-induced antineutrophil cytoplasmic antibody-associated vasculitis.
Article in Animal models and experimental medicine, 2026. 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
Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a systemic autoimmune disease characterized by small-vessel inflammation and the presence of ANCAs, which primarily target myeloperoxidase (MPO) and proteinase 3. Propylthiouracil (PTU), an antithyroid drug, is known as a causative drug of MPO-AAV. PTU induces the formation of DNase I-resistant neutrophil extracellular traps (NETs), which act as autoantigen sources and trigger the production of MPO-ANCAs. Although a rat model of PTU-induced AAV has been established, previous attempts to develop a corresponding mouse model have failed to replicate its histopathological features. In this study, we developed a novel murine model of PTU-induced AAV by enhancing neutrophil recruitment through intraperitoneal injection of thioglycolate, followed by intraperitoneal administration of phorbol 12-myristate 13-acetate and PTU to induce DNase I-resistant NETs. Freund's complete adjuvant was coadministered intradermally to amplify the immune response. This protocol resulted in abundant NET deposition in peritoneal tissues, elevated MPO-ANCA levels, and the development of pauci-immune glomerular lesions that closely resembled those observed in human AAV. Furthermore, a modified enzyme-linked immunosorbent assay (ELISA) reliably quantified murine MPO-ANCA levels. Thus, we established a novel murine model of PTU-induced AAV that recapitulates both the serological and histopathological features of the human disease. This model provides a valuable platform for investigating disease mechanisms, including NETs- and ANCA-mediated AAV pathogenesis.
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