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[未提及的物质]对MC903诱导的特应性皮炎小鼠模型中胸腺基质淋巴细胞生成素表达及辅助性T细胞分化的影响

Effects of on the Expression of Thymic Stromal Lymphopoietin and Differentiation of T Helper Cells in MC903-Induced Atopic Dermatitis Mouse Model.

作者信息

Zhou Xin, Cheng Zhuanggui, Yang Qintai, Ma Han, Xie Yang, Xu Zhe, Xia Jun, Chen Jian, Lu Chun, Feng Peiying

机构信息

Department of Dermatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.

Department of Allergy, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.

出版信息

Int J Microbiol. 2025 Apr 22;2025:3586621. doi: 10.1155/ijm/3586621. eCollection 2025.

Abstract

Atopic dermatitis (AD) is a chronic and inflammatory disease with an immunogenetic basis that can be triggered by extrinsic and intrinsic factors, including dysbiosis of the skin microbiota. The lipophilic is one of the dominant fungal species on the skin of AD patients. and the host pathophysiologic mechanism underlying its role in exacerbating AD symptoms remain to be elucidated. This experiment established a fungal overgrowth model by topical administration suspension of on BALB/c mice (M group) and MC903-induced AD model (AD+M group). Our results suggested that more severe AD-like lesions and higher dermatitis scoring were observed in the AD+M group compared with the AD group. The expression of TSLP mRNA in the tissue and serum IgE were highly increased in the AD group, while decreased significantly in the AD+M group. The expression levels of IL-17A and IL-22 in ear tissues and serum were significantly increased with stimulation, especially in the AD+M group. Meanwhile, the percentage of Th17 and Th22 cells in the spleen were positively correlated with IL-17A and IL-22 levels in the serum. In contrast, IFN- and IL-4 production were significantly decreased in the AD+M group compared with the AD group. This study demonstrated that overgrowing could aggravate AD symptoms and that IL-17A and IL-22 may be involved in the process. The promotion of IL-17A and IL-22 production induced by may restrain the development of TSLP and inhibit the Th1/Th2 type skin inflammation.

摘要

特应性皮炎(AD)是一种具有免疫遗传基础的慢性炎症性疾病,可由外在和内在因素引发,包括皮肤微生物群失调。亲脂性[真菌名称未给出]是AD患者皮肤中的主要真菌种类之一。其在加重AD症状中所起作用的宿主病理生理机制仍有待阐明。本实验通过对BALB/c小鼠局部给予[真菌名称未给出]悬浮液建立真菌过度生长模型(M组)以及MC903诱导的AD模型(AD+M组)。我们的结果表明,与AD组相比,AD+M组观察到更严重的AD样病变和更高的皮炎评分。AD组组织中TSLP mRNA的表达和血清IgE显著升高,而AD+M组则显著降低。经[真菌名称未给出]刺激后,耳部组织和血清中IL-17A和IL-22的表达水平显著升高,尤其是在AD+M组。同时,脾脏中Th17和Th22细胞的百分比与血清中IL-17A和IL-22水平呈正相关。相比之下,与AD组相比,AD+M组中IFN-[未给出具体类型]和IL-4的产生显著降低。本研究表明,[真菌名称未给出]过度生长可加重AD症状,且IL-17A和IL-22可能参与该过程。[真菌名称未给出]诱导的IL-17A和IL-22产生的促进作用可能会抑制TSLP的发展并抑制Th1/Th2型皮肤炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d44/12041643/2856474035f8/IJMICRO2025-3586621.001.jpg

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