壳寡糖抑制气道炎症,纤维化和粘液分泌在屋尘螨诱导的过敏模型。

IF 3.3 Q2 ALLERGY
Frontiers in allergy Pub Date : 2025-01-23 eCollection Date: 2025-01-01 DOI:10.3389/falgy.2025.1533928
Yun-Ho Kim, Chan-Ho Park, Ju Myung Kim, Yeo Cho Yoon
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引用次数: 0

摘要

背景:呼吸道过敏是一种严重的呼吸系统疾病,以炎症、粘液分泌过多和气道组织硬化为特征。屋尘螨(HDM)和细颗粒物诱导的刺激破坏T辅助1 (Th1)和T辅助2 (Th2)免疫系统,导致各种炎症细胞因子的分泌,导致以气道炎症为特征的免疫性呼吸系统疾病。壳寡糖(COS)以其抗氧化和抗炎特性而闻名。方法:人气道上皮细胞(BEAS-2B)在含COS浓度25-100µg/ml的DMEM/F12培养基中培养24 h。当浓度达到1000µg/ml时,未观察到细胞内毒性。细胞实验在COS浓度低于100µg/ml的条件下进行,动物实验在COS浓度低于100 mg/kg体重的条件下进行,持续4周。实验动物右肺组织样本用于基因和蛋白表达分析,对侧肺组织样本用于免疫组织化学分析。结果:COS通过抑制BEAS-2B细胞中炎性肿瘤坏死因子-α (TNF-α)、白细胞介素-1β (IL-1β)、白细胞介素-6 (IL-6)等主要细胞因子调节Th1免疫。在hdm诱导的过敏性呼吸道模型中,COS抑制气道周围炎症细胞浸润,抑制肺组织中Th1免疫细胞因子mRNA表达,同时降低核因子κB (NF-κB)相关蛋白表达。此外,结果证实了HDM激活的肥大细胞分泌的血液中免疫球蛋白E (IgE)水平的抑制,导致过敏性粘液分泌过多和气道硬化症的减少。结论:综上所述,COS可通过减轻HDM引起的炎症性变应性呼吸道疾病来改善气道阻力,并可作为调节黏液高分泌影响上皮细胞中Th1和Th2免疫系统平衡的物质。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Chitooligosaccharides suppress airway inflammation, fibrosis, and mucus hypersecretion in a house dust mite-induced allergy model.

Background: Respiratory allergy is a serious respiratory disorder characterized by inflammation, mucus hypersecretion, and airway tissue sclerosis. Disruption of the T helper 1 (Th1) and T helper 2 (Th2) immune systems by stimuli induced by house dust mites (HDM) and fine particulate matter leads to the secretion of various inflammatory cytokines, resulting in immune respiratory diseases characterized by airway inflammation. Chitooligosaccharides (COS) are known for their antioxidant and anti-inflammatory properties.

Methods: Human airway epithelial cells (BEAS-2B) were cultured in DMEM/F12 medium containing COS at concentrations of 25-100 µg/ml for 24 h. No intracellular toxicity was observed up to 1,000 µg/ml. Cell experiments were conducted at COS concentrations below 100 µg/ml, while animal experiments were performed at concentrations below 100 mg/kg body weight for 4 weeks. Samples of right lung tissue obtained from the experimental animals were used for gene and protein expression analysis, whereas samples of contralateral lung tissue were used for immunohistochemical analysis.

Results: COS regulated Th1 immunity by inhibiting major cytokines, including inflammatory tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), in BEAS-2B cells. In the HDM-induced allergic respiratory model, COS suppressed the infiltration of inflammatory cells around the airways and inhibited the mRNA expression of Th1 immune cytokines in lung tissues, while also reducing the expression of nuclear factor kappa B (NF-κB)-related proteins. Furthermore, the results confirmed the suppression of the levels of immunoglobulin E (IgE) in the blood secreted by mast cells activated by HDM, which led to a reduction in allergic mucus hypersecretion and airway sclerosis.

Conclusion: In summary, COS are thought to improve airway resistance by alleviating inflammatory allergic respiratory diseases caused by HDM and are regarded as substances that regulate the balance of the Th1 and Th2 immune systems in epithelial cells affected by mucus hypersecretion.

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