Yavuz S, Akdeniz T, Hancer V, Bicakcigil M, Can M, Yanikkaya-Demirel G
Department of Rheumatology, Istanbul Bilim University, Istanbul, Turkey.
Department of Immunology, Yeditepe University, Istanbul, Turkey.
Genes Immun. 2016 Sep;17(6):335-41. doi: 10.1038/gene.2016.28. Epub 2016 Jul 28.
Behcet's disease (BD) exhibits more severe disease course and higher mortality among male patients. However, underlying mechanisms of gender differences in clinical manifestations and disease severity are unclear. The aim of this study was to determine whether testosterone (T) has any role on BD pathogenesis. We studied peripheral blood mononuclear cells (PBMC) and neutrophils of BD patients and controls. Functional assay of neutrophils, cytokine measurements of culture supernatants and gene expressions on both cells were analyzed before and after T incubation. Neutrophils were significantly activated after incubation with T in only BD patients. Incubation with T caused significantly elevated interleukin (IL)-12 and IL-2 in BD. Gene expression of IL-10 was significantly downregulated after incubation with T in BD, especially in male patients. The same difference was observed in IL-10 levels in culture supernatant after T. Baseline TLR4 expression was significantly higher in BD patients compared to healthy donors (HC). Toll-like receptor (TLR) 4 expression on PBMC was significantly elevated in female BD patients. ERAP1 expressions of all patients and controls were decreased under the T effect but it differed significantly between BD vs HC. Baseline IL23R expression was higher in BD males compared with females but the difference disappeared after T. When BD patients were analyzed separately, baseline C-C motif chemokine receptor1 (CCR1), STAT4, TLR4 and KLRC4 expressions were lower in males. Despite immunosuppressive behavior in healthy subjects, T causes neutrophil hyperactivation and TH1 type immune alterations in BD patients. Our results suggest that T may have a role in BD pathogenesis by altering the expression level of IL-10, TLR4, ERAP1, CCR1.
白塞病(BD)在男性患者中表现出更严重的病程和更高的死亡率。然而,临床表现和疾病严重程度存在性别差异的潜在机制尚不清楚。本研究的目的是确定睾酮(T)在BD发病机制中是否起作用。我们研究了BD患者和对照组的外周血单个核细胞(PBMC)和中性粒细胞。在T孵育前后分析了中性粒细胞的功能测定、培养上清液的细胞因子测量以及两种细胞上的基因表达。仅在BD患者中,与T孵育后中性粒细胞被显著激活。与T孵育导致BD患者中白细胞介素(IL)-12和IL-2显著升高。在BD患者中,尤其是男性患者,与T孵育后IL-10的基因表达显著下调。T处理后,培养上清液中IL-10水平也观察到同样的差异。与健康供体(HC)相比,BD患者的基线Toll样受体4(TLR4)表达显著更高。女性BD患者PBMC上的Toll样受体(TLR)4表达显著升高。在T的作用下,所有患者和对照组的内质网氨肽酶1(ERAP1)表达均降低,但BD与HC之间存在显著差异。BD男性患者的基线IL23R表达高于女性,但T处理后差异消失。当分别分析BD患者时,男性患者的基线C-C基序趋化因子受体1(CCR1)、信号转导和转录激活因子4(STAT4)、TLR4和杀伤细胞凝集素样受体亚家族C成员4(KLRC4)表达较低。尽管在健康受试者中T具有免疫抑制作用,但它在BD患者中导致中性粒细胞过度活化和TH1型免疫改变。我们的结果表明,T可能通过改变IL-10、TLR4、ERAP1、CCR1的表达水平在BD发病机制中起作用。