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芽孢杆菌DU-106裂解物对2,4-二硝基氟苯诱导的特应性皮炎小鼠的治疗作用
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广东省重点领域研发计划(2020B020226008);国家现代农业产业技术体系(CARS-21)


Therapeutic effect of Bacillus sp. DU-106 lysate on 2,4-dinitrofluorobenzene-induced atopic dermatitis in mice
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    摘要:

    【背景】本团队前期研究发现芽孢杆菌DU-106具有良好的健康益处,但都是基于活菌的研究,对灭活菌的研究尚未开展。【目的】探究芽孢杆菌DU-106裂解物对特应性皮炎的治疗效果及作用机制。【方法】以2,4-二硝基氟苯诱导的特应性皮炎BALB/c小鼠为模型,通过病理学观察、免疫组化等手段研究其治疗效果,并测定NF-κB通路中基因与蛋白表达量,揭示其内在机制。【结果】芽孢杆菌DU-106裂解物有效缓解了特应性皮炎小鼠的病理学特征,减轻了肥大细胞的浸润,降低了免疫球蛋白E、肿瘤坏死因子-α (TNF-α)和干扰素-γ的含量(P<0.05)。芽孢杆菌DU-106裂解物可能是通过抑制NF-κB信号通路中TNF-α、IKKα和NF-κB基因表达水平和蛋白磷酸化而实现抗特应性皮炎效果。【结论】芽孢杆菌DU-106裂解物可作为一种后生元,对特应性皮炎具有积极的治疗作用。

    Abstract:

    [Background] Our research team have discovered that Bacillus sp. DU-106 has good health benefits in previous studies. However, the conclusion is based on the studies of living bacteria and the studies of inactivated bacteria remain to be carried out. [Objective] To investigate the effect and mechanism of Bacillus sp. DU-106 lysate in the treatment of atopic dermatitis. [Methods] Pathological observation and immunohistochemistry were employed to study the therapeutic effect of Bacillus sp. DU-106 lysate on the mouse model of 2,4-dinitrofluorobenzene-induced atopic dermatitis. The expression levels of the proteins involved in the nuclear factor kappa-B (NF-κB) signaling pathway were determined to reveal the mechanism. [Results] Bacillus sp. DU-106 lysate alleviated the pathological changes, reduced the infiltration of mast cells, and lowered the levels of immunoglobulin E, tumor necrosis factor-α (TNF-α), and interferon-γ (P<0.05) in the model mice. Furthermore, Bacillus sp. DU-106 lysate down-regulated the expression levels and inhibited the phosphorylation of TNF-α, inhibitory kappa B kinase α (IKKα), and NF-κB in the NF-κB signaling pathway in the model mice. [Conclusion] Bacillus sp. DU-106 lysate can be used as a probiotic with therapeutic effects on atopic dermatitis.

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赵文俊,张余威,李伟杰,赵超凡,李彦力,杜冰,黎攀. 芽孢杆菌DU-106裂解物对2,4-二硝基氟苯诱导的特应性皮炎小鼠的治疗作用[J]. 微生物学通报, 2023, 50(7): 2970-2982

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  • 收稿日期:2023-02-20
  • 录用日期:2023-03-22
  • 在线发布日期: 2023-07-10
  • 出版日期: 2023-07-20
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