NF-κB inhibition rescues Toll-like receptor 9 expression in human papillomavirus type 11 infected HaCaT cells

Zuolin Ying; Zhouwei Wu; Xiaojie Li; Hong Dang; Na Yin; Chuang Gao

NF-κB inhibition rescues Toll-like receptor 9 expression in human papillomavirus type 11 infected HaCaT cells

Int J Clin Exp Pathol. 2017 Sep 1;10(9):9460-9467. eCollection 2017.

Authors

Zuolin Ying¹, Zhouwei Wu¹, Xiaojie Li¹, Hong Dang¹, Na Yin¹, Chuang Gao¹

Affiliation

¹ Department of Dermatology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai, China.

PMID: 31966819
PMCID: PMC6965996

Abstract

Objectives: Toll-like receptors (TLRs) are related to human papillomavirus (HPV) infections including condyloma acuminatum (CA). This study was designed to investigate the mechanism of TLR9 and nuclear factor κB (NF-κB) in CA.

Methods: Expression of TLR9 protein in CA patients was detected and compared with those in CA relapse-free (CaRF) patients and normal control. HaCaT cells were transfected with HPV11 genome and NF-κB p65 siRNA or IκB kinase inhibitor BMS345541. Expression of NF-κB and TLR9 were detected using both PCR and Western blot methods.

Results: TLR9 was downregulated in CA specimens as compared to CaRF and normal controls. HPV11 transfection into HaCaT (HPV11.HaCaT) cells reduced TLR9 expression and activated NF-κB p65 expression. However, administration of NF-κB p65 siRNA or IκB kinase inhibitor BMS345541 significantly inhibited NF-κB p65 expression and rescued the expression of TLR9.

Conclusion: Inhibition of NF-κB activation could rescue TLR9 expression in HPV11.HaCaT cells. TLR9/NF-κB mechanism may provide new target for clinical treatment of CA.

Keywords: Condyloma acuminatum; HPV11; HaCaT; NF-κB.