IL-1β induced by PRRSV co-infection inhibited CSFV C-strain proliferation via the TLR4/NF-κB/MAPK pathways and the NLRP3 inflammasome

Highly pathogenic PRRSV upregulates IL-13 production through nonstructural protein 9–mediated inhibition of N6-methyladenosine demethylase FTO

“…Recent studies have revealed that PRRSV infection can modulate innate antiviral defense, cause immunosuppression, alleviate inflammatory response, and alter pathological reaction during lung damage. Besides, PRRSV infection can cause excessive secretion of proinflammatory cytokines and chemokines, including IL-1β, IL-4, IL-6, IL-8, IL-12, IL-17, and TNF-α ( 3 , 12 , 54 , 55 ). The high level of IL-1β induced by PRRSV infection can significantly inhibit the replication and release of classical swine fever virus C strain proliferation.…”

“…The high level of IL-1β induced by PRRSV infection can significantly inhibit the replication and release of classical swine fever virus C strain proliferation. The induction of IL-1β by PRRSV is presumed to be mediated by TLR4–NF-κB–MAPK signaling pathways and NLRP3 inflammasome in host cells ( 3 ). PRRSV-2 has been noted to be involved in the regulation of lung injury by targeting STAT1 and TNF-α, which might be associated with mir-331-3p/mir-210 ( 6 ).…”

“…It causes reproductive disorders and breathing difficulties in pigs, generating huge economic loss to the swine industry ( 2 ). The PRRSV genome contains 11 ORFs, encoding eight structural proteins and 16 nonstructural proteins (nsp), each possessing diverse functions in various steps of infection, replication, virulence, and virus–host interactions ( 3 , 4 , 5 , 6 , 7 , 8 ). Immunosuppression after PRRSV infection may contribute to inefficient innate and acquired immune responses, modulating the expression and release of inflammatory and/or anti-inflammatory factors, upregulating immunosuppressive cytokines expression, and allowing the viruses to rapidly reproduce and cause disease ( 9 , 10 , 11 , 12 ).…”

Predicting the efficacy of glucocorticoids in pediatric primary immune thrombocytopenia using plasma proteomics

“…By binding to the extracellular structural domain of TLR4, it activates NF-kB signalling, subsequently inducing the release of pro-inflammatory cytokines from macrophages. The involvement of FETUA in TLR activation and consequent inflammatory signalling can contribute to glucocorticoid resistance (39,40). Although fewer studies have been conducted on FETUB, its structural homology to FETUA suggests a potentially similar role.…”

miR-642a-5p increases glucocorticoid sensitivity by suppressing the TLR4 signalling pathway in THP-1 cells

“…Bioinformatics software predicted that TLR4 is a target gene of miR-642a-5p. Current studies suggest that the TLR4/NF-κB pathway is closely related to regulation of the expression of inflammatory cytokines [ [28] , [29] , [30] ]. Increased expression of IL-1β, IL-6, IL-12, and TNF-α has been detected in active UC, and this increased expression is associated with the severity of inflammation [ [31] , [32] , [33] ].…”