Department of Allergy and Clinical Immunology, the Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang Province 310009, China.
State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products, Ningbo University, Ningbo, Zhejiang Province 315211, China; Laboratory of Biochemistry and Molecular Biology, School of Marine Sciences, Meishan Campus, Ningbo University, Ningbo, Zhejiang Province 315832, China.
Life Sci. 2024 Jan 1;336:122310. doi: 10.1016/j.lfs.2023.122310. Epub 2023 Nov 25.
Qipian® is a commercialized agent composed of extracts of three genera of commensal bacteria, and its mechanism of action on asthma is unclear. This study aimed to examine the impact of Qipian® on airway inflammation and investigate the underlying mechanisms.
Qipian® or dexamethasone (DEX) was administered before OVA challenge in an ovalbumin-induced asthma mouse model, and then asthmatic symptoms were observed and scored. Samples of lung tissues, blood, and bronchoalveolar lavage fluid (BALF) were collected, and eosinophils (Eos), immunoglobins (Igs), and type 1 T helper (Th1)/Th2 cell cytokines were measured. Mucus production in the lung was assessed by periodic acid-Schiff (PAS) staining. The effects of Qipian® on dendritic and T regulatory (Treg) cells were investigated using flow cytometry.
The short-term administration of Qipian® significantly inhibited the cardinal features of allergic asthma, including an elevated asthmatic behaviour score, airway inflammation and immune response. Histological analysis of the lungs showed that Qipian® attenuated airway inflammatory cell infiltration and mucus hyperproduction. Qipian® restored Th1/Th2 imbalance by decreasing interleukin (IL)-4, IL-5, and IL-13 while increasing interferon (IFN)-γ and IL-10. Further investigation revealed that Qipian® treatment induced the upregulation of CD4CD25Foxp3 Treg cells and CD103 DCs and downregulation of tachykinins neurokinin A (NKA) and NKB in the lung.
Our findings suggested that short-term treatment with Qipian® could alleviate inflammation in allergic asthma through restoring the Th1/Th2 balance by recruiting Treg cells to airways and inducing the proliferation of CD103 DCs, which actually provides a new treatment option for asthma.
奇片®是一种由三种共生菌属提取物组成的商业化制剂，其作用机制尚不清楚。本研究旨在探讨奇片®对气道炎症的影响及其潜在机制。
在卵清蛋白诱导的哮喘小鼠模型中，在 OVA 攻击前给予奇片®或地塞米松（DEX），然后观察和评分哮喘症状。收集肺组织、血液和支气管肺泡灌洗液（BALF）样本，测量嗜酸性粒细胞（Eos）、免疫球蛋白（Igs）和 1 型 T 辅助（Th1）/Th2 细胞细胞因子。用过碘酸-Schiff（PAS）染色评估肺内粘液生成。用流式细胞术研究奇片®对树突状和 T 调节（Treg）细胞的影响。
奇片®的短期给药显著抑制了过敏性哮喘的主要特征，包括哮喘行为评分升高、气道炎症和免疫反应。肺组织学分析表明，奇片®减轻了气道炎症细胞浸润和粘液过度产生。奇片®通过降低白细胞介素（IL）-4、IL-5 和 IL-13，同时增加干扰素（IFN）-γ和 IL-10，恢复了 Th1/Th2 失衡。进一步研究表明，奇片®治疗诱导了 CD4CD25Foxp3 Treg 细胞和 CD103 DC 的上调，并下调了肺中的速激肽神经激肽 A（NKA）和 NKB。
我们的研究结果表明，奇片®的短期治疗可以通过招募 Treg 细胞到气道并诱导 CD103 DC 的增殖来恢复 Th1/Th2 平衡，从而减轻过敏性哮喘的炎症，为哮喘提供了一种新的治疗选择。
