ArticleInternational journal of clinical and experimental pathology2017
NF-κB inhibition rescues Toll-like receptor 9 expression in human papillomavirus type 11 infected HaCaT cells.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors at 1 institution in 1 country.
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Abstract
objectivesToll-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.
methodsExpression 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.
resultsTLR9 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.
conclusionInhibition 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.
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Identifiers
31966819PMC6965996W3026610757What OpenQuestion holds
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