Zeng Wucheng, Wang Yihan, Cao Yi, Xing Fengling, Yang Xiaohong
Department of Dermatology and Venereology, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310007, P.R. China.
Department of Dermatology, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, P.R. China.
Exp Ther Med. 2023 Apr 24;25(6):278. doi: 10.3892/etm.2023.11976. eCollection 2023 Jun.
The aim of the present study was to investigate the influence of stimulating food (SF), a Traditional Chinese Medicine term for a high protein, high fat diet, on psoriasis exacerbation. It was hypothesized that SF disposed psoriasis-like aggravation might be related to inflammatory pathways induction via gut dysbiosis. In the present study, mice were fed either an SF or normal diet for 4 weeks. In the last week, their back hair was removed to establish psoriasis-like dermatitis by imiquimod. After sacrifice, blood samples, alimentary tissues and skin lesions were collected and tested by enzyme-linked immunosorbent assay, western blotting, immunohistochemistry and immunofluorescence. Compared with normal diet groups, body weight and blood glucose of SF diet mice were not increased, but they exhibited higher modified Psoriasis Area and Severity Index scores and corresponding epithelial hyperproliferation. Unexpectedly, skin lesions showed abnormal lower protein expressions of Notch and TLR-2/NF-κB p65 signaling pathway, which was attributable to severe skin damage. No difference was observed in the structure and inflammatory cell infiltration of the gut between groups. Instead, macrophage polarization (M1/M2) in the gut of the SF diet group marked by high expression of CD11b (a marker of macrophage, M1) and mild low expression of MRC1 (a marker of macrophage, M2), which resulted in increased TNF-α, decreased IL-10, IL-35, and unchanged IL-17 in serum. Furthermore, serum derived from SF diet mice promoted translocation of NF-κB p65 in HaCaT cells, which indirectly suggested a systemic inflammation. These results suggested that mice fed a continuous SF diet for a time could change gut macrophage polarization, which secretes proinflammatory cytokines into blood circulation. Once transported to skin lesions, these cytokines activate psoriasis tissue resident immune cells and present as psoriasis exacerbation.
本研究的目的是探讨刺激性食物(SF,中医术语,指高蛋白、高脂肪饮食)对银屑病加重的影响。研究假设,SF导致的银屑病样加重可能与肠道菌群失调诱导的炎症途径有关。在本研究中,将小鼠分为两组,分别喂食SF饮食或正常饮食4周。在最后一周,去除小鼠背部毛发,通过咪喹莫特诱导建立银屑病样皮炎。处死后,采集血液样本、消化道组织和皮肤病变组织,采用酶联免疫吸附测定、蛋白质免疫印迹法、免疫组织化学和免疫荧光法进行检测。与正常饮食组相比,SF饮食组小鼠的体重和血糖没有增加,但银屑病面积和严重程度指数评分更高,且伴有相应的上皮细胞过度增殖。出乎意料的是,皮肤病变显示Notch和TLR-2/NF-κB p65信号通路的蛋白质表达异常降低,这归因于严重的皮肤损伤。两组之间肠道结构和炎症细胞浸润没有差异。相反,SF饮食组小鼠肠道中的巨噬细胞极化(M1/M2)以CD11b(巨噬细胞M1的标志物)高表达和MRC1(巨噬细胞M2的标志物)轻度低表达为特征,导致血清中TNF-α升高,IL-10、IL-35降低,IL-17不变。此外,SF饮食组小鼠的血清促进了HaCaT细胞中NF-κB p65的转位,这间接提示了全身炎症。这些结果表明,持续喂食SF饮食一段时间的小鼠可改变肠道巨噬细胞极化,使其向血液循环中分泌促炎细胞因子。一旦这些细胞因子转运至皮肤病变部位,就会激活银屑病组织驻留免疫细胞,导致银屑病加重。