Porcine reproductive and respiratory syndrome (PRRS) is associated with the endemic outbreak of fever, anorexia, and abortion in pregnant sows, resulting in an enormous economic impact on the global swine industry. Current mainstream prophylactic agents and therapies have been developed to prevent PRRSV infection; however, they have limited efficacy. Therefore, there is an urgent need to develop novel antiviral strategies to prevent PRRSV infection and transmission. The identification of new PRRSV entry mediators, such as MYH9 and HSPA8; viral apoptotic mimicry; and TIM-induced macropinocytosis, to facilitate infection has led to a novel molecular understanding of the PRRSV infection mechanism, which can be utilized in the development of prophylactic agents and therapies for PRRSV infection. Polyphenols, complex chemical molecules with abundant biological activities derived from microorganisms and plants, have demonstrated great potential for controlling PRRSV infection via different mechanisms. To explore new possibilities for treating PRRSV infection with polyphenols, this review focuses on summarizing the pathogenesis of PRRSV, reviewing the potential antiviral mechanisms of polyphenols against PRRSV, and addressing the challenges associated with the widespread use of polyphenols.

Porcine reproductive and respiratory syndrome virus (PRRSV), the most economically important infectious disease of pigs, elicits poor innate and adaptive immune responses. Soluble CD83 (sCD83), a secretion from various immune cell populations, especially MoDCs, is involved in negatively regulating the immune response. We speculate sCD83 may be a critical factor in the process of PRRSV-coordinated macrophage polarization. In this study, we found that PAMs co-cultured with PRRSV-infected MoDCs inhibited the M1 macrophage while enhancing the M2 macrophage. This was accompanied by a decrease in the pro-inflammatory cytokine TNF-α and iNOS and an increase in the anti-inflammatory cytokine IL-10 and Arg1. Meanwhile, sCD83 incubation causes the same specific effects lead to a switch in macrophage from M1 to M2. Neutralization of sCD83 removes the inhibitory effects of PRRSV on PAMs. Using reverse genetics, we generated recombinant PRRSVs with mutations in N protein, nsp1α, and nsp10 (knockout sCD83-concerned key amino acid site). Four mutant viruses lost the suppression of M1 macrophage markers, in contrast to the restriction of the upregulation of M2 macrophage markers. These findings suggest that PRRSV modulates the switch of macrophage polarization from M1 to M2 by upregulating the MoDC-induced secretion of CD83, providing new insights into the mechanism by which PRRSV regulates host immunity.

Chronic diabetic wounds are characterized by persistent oxidative stress and microbial infections, leading to delayed healing and tissue repair. While elevated reactive oxygen species (ROS) levels can provide bactericidal effects, uncontrolled oxidative stress simultaneously impairs tissue regeneration. Thus, precise redox modulation that balances antimicrobial efficacy with tissue regeneration is critical for effective wound therapy. Herein, we developed a phytochemical nanozymes system by integrating ferulic acid (FA) with cerium oxide nanoparticles (CeO₂), enabling precise redox modulation to balance antimicrobial efficacy with tissue regeneration. Structural analysis confirmed the uniform dispersion and pH-responsive release of FA and Ce ions, facilitating targeted redox modulation. The FA-CeO₂ nanozymes exhibited potent antioxidant activity through Ce³⁺/Ce⁴⁺ cycling and FA-mediated radical scavenging, effectively mitigating oxidative stress while promoting bacterial clearance against S. aureus and E. coli. Furthermore, FA-CeO₂ significantly enhanced Nrf2/HO-1 pathway activation, leading to upregulated VEGF/CD31 expression, accelerated cell proliferation, and enhanced collagen deposition in vitro. In vivo, FA-CeO₂ facilitated wound closure, reduced bacterial burden, and improved tissue regeneration in acute and diabetic wound models, with minimal cytotoxicity and excellent biocompatibility. These findings highlight the critical role of precise redox modulation in balancing antibacterial and regenerative therapy, positioning phytochemical nanozymes as a dual-modality platform for effective wound therapy and advancing nanomedicine strategies targeting oxidative stress and tissue repair.

Although advances in nanomedicine using nanoparticles (NPs) derived from natural compounds have provided us with much insight into how to recover from wound infections, exploring the wound healing pathway remains a new perspective that has attracted significant interest in addressing wound complications challenges. Here, we harnessed the therapeutic potential of novel selenium nanoparticles (SeNPs) derived from Purple sweet potato (PSp) extracts to promote wound healing through the regulation of pyroptosis-related pathways. PSp-SeNPs, with an average particle size of 80–100 nm, demonstrated significant antibacterial activity against S. aureus and MRSA clinical pathogens. The mechanism involves impairment of bacterial growth, biofilm formation, and metabolic processes through ATP depletion. Moreover, PSp-SeNPs impairs NLRP3-mediated pyroptosis including p-IκBα, p-NF-κB, IL-18, and IL-1β. This regulatory effect decreases inflammatory cytokines IL-6 and TNF-α while promoting angiogenesis and collagen formation through increased expression levels of TGF-β, VEGFA, and CD31, thus accelerating wound healing. In vivo assessments confirmed that PSp-SeNPs significantly enhanced wound healing without adverse effects, indicating their high biocompatibility and bioavailability. This groundbreaking study elucidates the therapeutic potential of PSp-based selenium nanoparticles, facilitating the development of precise and efficient treatment strategies for wound healing and diverse medical applications.