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

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 ?B (NF-?B) 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-?B p65 siRNA or I?B kinase inhibitor BMS345541. Expression of NF-?B 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-?B p65 expression. However, administration of NF-?B p65 siRNA or I?B kinase inhibitor BMS345541 significantly inhibited NF-?B p65 expression and rescued the expression of TLR9. CONCLUSION:Inhibition of NF-?B activation could rescue TLR9 expression in HPV11.HaCaT cells. TLR9/NF-?B mechanism may provide new target for clinical treatment of CA.

SUBMITTER: Ying Z

PROVIDER: S-EPMC6965996 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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

Ying Zuolin Z Wu Zhouwei Z Li Xiaojie X Dang Hong H Yin Na N Gao Chuang C

International journal of clinical and experimental pathology 20170901 9

<h4>Objectives</h4>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.<h4>Methods</h4>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 N ...[more]

PMID: 31966819

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Project description:Psoriasis is a chronic inflammatory skin condition with numerous causes, including genetic, immunological and infectious factors. The course of psoriasis is long and recurrence is common; pathogenesis is not completely understood. However, there is an association between advancement of psoriasis and aberrant microRNA (miR or miRNA)‑155 expression. Through bioinformatics, the present study aimed to analyze the differentially expressed genes and miRNAs in psoriasis and its biological mechanism and function psoriatic inflammation. First of all, differentially expressed genes (DEGs) and miRNAs (DEMs) in patients with psoriasis were identified using GEO2R interactive web application. A psoriasis inflammatory model was established using lipopolysaccharide (LPS)‑treated HaCaT keratinocytes, which were transfected with miR‑155 mimic or inhibitor. Cell Counting Kit‑8 was used for the assessment of cell viability and proliferation, and changes in the cell cycle were examined using flow cytometry. ELISA and reverse transcription‑quantitative PCR (RT‑qPCR) were used to detect the expression levels of the inflammatory factors IL‑1β and IL‑6. The dual‑luciferase reporter assay was used to verify the targeting association between miR‑155‑5p and IFN regulatory factor 2 binding protein 2 (IRF2BP2). To verify the targeting association of miR‑155 and the IRF2BP2/kruppel‑like factor 2 (KLF2)/NF‑κB signaling pathway, expression levels of IRF2BP2, KLF2 and p65 were identified by RT‑qPCR and western blotting. IRF2BP2 levels were also confirmed by immunofluorescence, in conjunction with bioinformatics database analysis. Overexpression of miR‑155 inhibited proliferation of HaCaT cells and increased the number of cells in S phase and decreasing number of cells in G1 and G2 phase. In the LPS‑induced inflammatory state, miR‑155 overexpression heightened the inflammatory response of HaCaT cells while inhibition of miR‑155 lessened it. Suppression of inflammatory cytokine expression by miR‑155‑5p inhibitor was reversed by knockdown of IRF2BP2. miR‑155 was shown to interact with IRF2BP2 to negatively regulate its expression, leading to decreased KLF2 expression and increased p65 expression and secretion of inflammatory factors, intensifying the inflammatory response of HaCaT cells. Therefore, miR‑155 may contribute to development of psoriasis by inducing tissue and cell damage by increasing the inflammatory response of HaCaT cells via the IRF2BP2/KLF2/NF‑κB pathway. In conclusion, the results of the present study offer novel perspectives on the role of miR‑155 in the onset and progression of psoriasis.

Dataset Information

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

Publications

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

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