What question did this study set out to answer?

The research aims to explore the metabolic and inflammatory responses of renal tissues in chickens infected with IBV.

May 25, 2026Veterinary Research0 citationsOpen Access

Avian coronaviruses induce inflammatory responses by activating p38/MAPK signaling and NLRP3/caspase-1 inflammasomes through sphingosine-1-phosphate receptor 1

HXHongtao XiaoSouth China Agricultural University SYSiyao YuSouth China Agricultural University SLShijing LiSouth China Agricultural University

Key Points

The research aims to explore the metabolic and inflammatory responses of renal tissues in chickens infected with IBV.
Applied metabolomic analysis to kidney tissues from IBV-infected SPF chickens.
Investigated metabolic alterations and proinflammatory cytokine expression.
Studied the S1P-S1PR1 signaling pathway and its effect on p38/MAPK and NLRP3 inflammasome activation.
Significant downregulation of amino acids and their derivatives observed at 7 dpi, impacting IBV replication.
Marked elevation in L-glutamine, D-mannose 1-phosphate, and D-galacturonate levels, indicating their role in energy utilization during infection.
S1P was identified as upregulated, enhancing p38/MAPK pathway activation and NLRP3/caspase-1 inflammasome, leading to increased IL-1β and IL-18 expression.

Abstract

Abstract Infectious bronchitis virus (IBV), a member of the γ-coronavirus genus within the Coronaviridae family, is a major pathogenic threat to the global poultry industry. Most IBV infections induce severe renal pathological lesions in chickens, yet the renal metabolic perturbations triggered by IBV infection remain largely elusive. Herein, we applied a metabolomic approach to characterize the metabolic profiles of kidney tissues from IBV-infected specific-pathogen-free (SPF) chickens. IBV infection caused profound alterations in the renal metabolome, encompassing amino acids and their derivatives, energy metabolites, and lipid molecules. Most amino acids and their derivatives were significantly downregulated at 7 days post-infection (dpi), indicating that IBV usurps host amino acid pools to support its own replication in SPF chickens. In addition, the levels of L-glutamine, D-mannose 1-phosphate, and D-galacturonate were markedly elevated post-infection, implying their potential roles in mediating host energy utilization and facilitating viral replication during IBV infection. Subsequently, sphingosine-1-phosphate (S1P)—a key bioactive lipid molecule—was identified as a prominently upregulated metabolite in IBV-infected kidney tissues. Follow-up functional experiments revealed that IBV infection upregulates the S1P-S1PR1 signaling axis, and concomitantly activates the p38/JNK/MAPK pathway as well as the NLRP3/caspase-1 inflammasome. Notably, S1PR1 was found to modulate the p38/MAPK signaling pathway and NLRP3/caspase-1 inflammasome, thereby regulating the expression of the proinflammatory cytokines IL-1β and IL-18. Collectively, our study delineates the comprehensive renal metabolic landscape of chickens in response to IBV infection and identifies S1PR1 as a pivotal regulatory target of IBV-induced renal inflammation. These findings provide novel mechanistic insights for the development of preventive and therapeutic strategies targeting metabolic signaling pathways against IBV infection.

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