罗伐他汀干预慢性乙型肝炎(CHB)患者可通过芳基烃受体(AHR)扩增 CD14+ CD16- 经典单核细胞

Immuno Pub Date : 2024-05-17 DOI:10.3390/immuno4020011
Mina Rahmati, Mojtaba Zare Ebrahimabad, Alale Langari, Ali Najafi, Shohreh Taziki, Alireza Norouzi, M. Teimoorian, M. Khorasani, Saeed Mohammadi
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引用次数: 0

摘要

慢性乙型肝炎(CHB)给治疗带来了挑战,治疗反应和疾病预后往往取决于免疫反应,尤其是单核吞噬细胞。单核细胞可分化成受 AHR 影响的各种亚群。他汀类药物具有调节炎症的作用,可能会通过激活 AHR 影响单核细胞的功能。本研究探讨了洛伐他汀(RSV)对慢性阻塞性肺病患者单核细胞亚型、炎症指标和 AHR 的影响。15 名慢性阻塞性肺病患者被随机分配到每天服用 20 毫克 RSV 或安慰剂,为期三个月。流式细胞术评估了 CD14+ CD16-(典型)、CD14+ CD16+(中间)和 CD14dim CD16+(巡逻)单核细胞亚型,以及每个亚型的 AHR 水平。ELISA 对细胞因子 IL-6、IFN-γ、IL-12、IL-10、TNF-α、TGF-β 和 IL-1β 进行了量化。RSV 扩增了 CHB 患者的 CD14+ CD16- 经典单核细胞,减少了 CD14+ CD16+ 中间单核细胞,同时增加了所有亚群中 AHR+ 细胞的百分比。RSV 治疗上调了关键的 AHR 靶基因(Cyp1a1、Cyp1b1 和 ARNT),表明 AHR 信号被强有力地激活。它还降低了促炎细胞因子(IL-6、IFNγ、IL-12、TNF-α)的水平,提高了抗炎细胞因子(IL-10、TGF-β)的水平。因此,RSV 可通过激活 AHR 改变慢性阻塞性肺病患者的单核细胞亚型,从而调节免疫反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Rosuvastatin Intervention in Patients with Chronic Hepatitis B (CHB) Expands CD14+ CD16− Classical Monocytes via Aryl Hydrocarbon Receptor (AHR)
Chronic hepatitis B (CHB) poses treatment challenges, with treatment response and disease outcome often determined by the immune response, particularly mononuclear phagocytes. Monocytes can differentiate into various subpopulations influenced by AHR. Statins, known for inflammation modulation, may impact monocyte function via AHR activation. This study explored rosuvastatin (RSV)’s effects on monocyte subtypes, inflammatory markers, and AHR in CHB patients. Fifteen CHB patients were randomly assigned to receive either 20 mg RSV or a placebo daily for three months. Flow cytometry assessed CD14+ CD16− (classical), CD14+ CD16+ (intermediate), and CD14dim CD16+ (patrolling) monocyte subtypes, along with AHR levels in each subset. ELISA quantified cytokines IL-6, IFN-γ, IL-12, IL-10, TNF-α, TGF-β, and IL-1β. RSV expanded CD14+ CD16− classical and reduced CD14+ CD16+ intermediate monocytes in CHB patients while increasing AHR+ cell percentages in all subsets. RSV treatment upregulated key AHR target genes (Cyp1a1, Cyp1b1, and ARNT), indicating robust AHR signaling activation. It also reduced pro-inflammatory cytokine levels (IL-6, IFNγ, IL-12, TNF-α) and elevated anti-inflammatory cytokines (IL-10, TGF-β). Thus, RSV may modulate the immune response by altering monocyte subtypes in CHB patients via AHR activation.
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