IL-33/ST2信号轴在VZV感染致炎中的作用及其对带状疱疹后遗神经痛的调控OA

Objective To investigate the regulatory role and underlying mechanisms of the interleukin-33(IL-33)/growth stimulating protein 2(ST2)signaling pathway in varicella-zoster virus(VZV)-induced inflammatory re-sponses,and to elucidate its involvement in the development of postherpetic neuralgia(PHN).Methods An in vitro VZV infection model was established using African green monkey kidney fibroblast(CV-1)cells.After successful viral infection,cells were treated with different concentrations of IL-33 and ST2 for 48 hours.Protein expression levels of in-flammation-and signaling-related molecules-including NLRP3,IL-33,NF-κB,p65,phosphorylated NF-κB(p-NF-κB),phosphorylated p65(p-p65),and phosphorylated IκB(p-IκB)-were analyzed by Western blotting.Immunofluorescence staining was performed to evaluate the expression and localization of key signaling proteins.Results Western blot analysis demonstrated that the expression levels of NLRP3,IL-33,NF-κB,p65,p-NF-κB,p-p65,and p-IκB were significantly increased in both IL-33-and ST2-treated groups compared with the normal saline con-trol group(P＜0.05,P＜0.01,or P＜0.001).Consistently,immunofluorescence analysis revealed significantly elevat-ed expression of NLRP3,phosphorylated NF-κB,and phosphorylated IκB in the IL-33 and ST2 treatment groups rela-tive to controls(P＜0.05,P＜0.01,or P＜0.001).Conclusion An in vitro PHN-related inflammatory model was established using VZV-infected CV-1 cells,in which NLRP3 expression was positively associated with inflammatory ac-tivation.Abnormal activation of the IL-33/ST2 signaling axis was observed,suggesting that this pathway may play a criti-cal regulatory role in the pathogenesis of PHN,potentially through modulation of inflammasome activation and NF-κB sig-naling.