Validating Distinction between Respiratory and Nephropathogenic Infectious Bronchitis Virus Strains via Chicken Tracheal Organ Culture: Insights on Innate Immune Enhancement and the COX-2/PGE2 Pathway

The findings reveal distinct patterns of COX-2 expression, PGE2 production, and immune responses associated with different IBV strains, highlighting the complexity of host-virus interactions.

•IBV genome load and protein expression peaked at 12 and 24 hpi, respectively.

•Conn A5968-infected TOCs exhibited continuous COX-2 expression for up to 24 hpi, extended PGE2 production up to 48 hpi, and reduced inflammatory cytokine expression.

•In contrast, DMV/1639-infected TOCs displayed heightened inflammatory cytokine expression, brief COX-2 expression, and PGE2 production.

•Treatment with IFN-γ, SC-236, PGE2 receptor inhibitors, or JAK inhibitors reduced IBV infection and lesion scores,

•while exogenous PGE2 or IFN-γ pretreatment with a JAK-2 inhibitor augmented infection.

 Our study unravels intricate distinctions between the IBV respiratory strain Conn A5968 and the IBV nephropathogenic strain DMV/1639 in IBV-infected tracheal organ explants, shedding light on their divergent pathogenesis.

The IBV Conn A5968, despite exhibiting higher replication, demonstrated potential immune evasion strategies, marked by lower pro-inflammatory cytokine markers, possibly facilitated by an activated COX-2/PGE2 pathway.

Conversely, the robust innate immune responses observed in IBV DMV/1639 infection, reflected by heightened pro-inflammatory cytokine expressions, seemed instrumental in restricting its replication and promoting clearance from tracheal explants.