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膳食益生元诱导的半乳糖凝集素-9 调节免疫调节,减轻 1-氯-2,4-二硝基苯(DNCB)处理的 NC/Nga 小鼠的特应性皮炎症状。

Galectin-9 Induced by Dietary Prebiotics Regulates Immunomodulation to Reduce Atopic Dermatitis Symptoms in 1-Chloro-2,4-Dinitrobenzene (DNCB)-Treated NC/Nga Mice.

机构信息

Department of Animal Resources Technology, Gyeongnam National University of Science and Technology, Jinju 52725, Republic of Korea.

Department of Animal Science, Chonnam National University, Gwangju 61186, Republic of Korea 3 Department of Animal Science & Biotechnology, Gyeongnam National University of Science and Technology, Jinju 52725, Republic of Korea.

出版信息

J Microbiol Biotechnol. 2020 Sep 28;30(9):1343-1354. doi: 10.4014/jmb.2005.05017.

DOI:10.4014/jmb.2005.05017
PMID:32699202
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9745654/
Abstract

Atopic dermatitis (AD) is a skin disorder that causes chronic itch. We investigated the inhibitory effects of a mixture of prebiotic short-chain galacto-oligosaccharides and long-chain fructooligosaccharides (scGOS/lcFOS), inulin, or β-glucan on AD development in 1-chloro-2,4- dinitrobenzene (DNCB)-treated NC/Nga mice. Mice were randomly assigned to six groups: untreated mice, AD control, positive control (DNCB-treated NC/Nga mice fed a dietary supplement of Zyrtec), and DNCB-treated NC/Nga mice fed a dietary supplement of prebiotics such as scGOS/lcFOS (T1), inulin (T2), or β-glucan (T3). The prebiotic treatment groups (T1, T2, and T3) showed suppression of AD symptoms, Th2 cell differentiation, and AD-like skin lesions induced by DNCB. In addition, prebiotic treatment also reduced the number of microorganisms such as , which is associated with AD symptoms, and increased the levels of and , which are associated with alleviation of AD symptoms. Our findings demonstrate the inhibitory effects of prebiotics on AD development by improving the Th1/Th2 cytokine balance and beneficial symbiotic microorganisms in in vitro and in vivo models.

摘要

特应性皮炎(AD)是一种引起慢性瘙痒的皮肤疾病。我们研究了短链半乳糖寡糖和长链菊粉混合物、菊糖或β-葡聚糖对 1-氯-2,4-二硝基苯(DNCB)处理的 NC/Nga 小鼠 AD 发展的抑制作用。将小鼠随机分为六组:未处理的小鼠、AD 对照组、阳性对照(DNCB 处理的 NC/Nga 小鼠用 Zyrtec 进行饮食补充)和 DNCB 处理的 NC/Nga 小鼠用 scGOS/lcFOS(T1)、菊糖(T2)或β-葡聚糖(T3)进行饮食补充。结果显示,益生元治疗组(T1、T2 和 T3)抑制了 DNCB 诱导的 AD 症状、Th2 细胞分化和 AD 样皮肤损伤。此外,益生元治疗还减少了与 AD 症状相关的微生物如 的数量,并增加了与 AD 症状缓解相关的 和 的水平。我们的研究结果表明,益生元通过改善体外和体内模型中的 Th1/Th2 细胞因子平衡和有益共生微生物,对 AD 的发展具有抑制作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/f7f1d4838555/JMB-30-9-1343-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/6c1d9a523db4/JMB-30-9-1343-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/37997dec4cb9/JMB-30-9-1343-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/72eabc2a7de2/JMB-30-9-1343-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/b9f1e040e762/JMB-30-9-1343-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/b5821937d34c/JMB-30-9-1343-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/f7f1d4838555/JMB-30-9-1343-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/6c1d9a523db4/JMB-30-9-1343-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/37997dec4cb9/JMB-30-9-1343-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/72eabc2a7de2/JMB-30-9-1343-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/b9f1e040e762/JMB-30-9-1343-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/b5821937d34c/JMB-30-9-1343-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d08/9745654/f7f1d4838555/JMB-30-9-1343-f6.jpg

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