Avian coronavirus IBV-induced activation of the NLRP3–Caspase-1–IL-1β axis in renal collecting ducts contributes to nephropathogenesis

<i>In vivo</i> studies in chickens demonstrate that the activation of the NLRP3 inflammasome is a key driver of renal injury during infectious bronchitis virus (IBV) infection. Pharmacological inhibition of NLRP3 significantly alleviates renal inflammation and tissue damage without affecting viral replication, highlighting the central role of host inflammatory responses in disease progression. Importantly, we report for the first time that NLRP3 activation is predominantly localized to AQP2-positive collecting ducts, a nephron segment essential for uric acid excretion and electrolyte balance. IBV infection reprograms these epithelial cells into a pro-inflammatory, metabolically dysregulated state, promoting urate crystal formation and amplifying tissue injury. These findings reveal a spatially confined epithelial-immune axis of coronavirus-induced renal pathology and suggest new avenues for targeted intervention.