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益生元甘露聚糖对过敏性哮喘小鼠模型的有益作用。

Beneficial Effects of Prebiotic Mannan on Allergic Asthma Mouse Models.

机构信息

Department of Pediatrics, University of Tennessee Health Science Center (UTHSC) and Children's Foundation Research Institute, Le Bonheur Children's Hospital, Memphis, TN, USA.

Department of Pediatrics and Hematology-Oncology, Baylor College of Medicine and Texas Children's Cancer Center, Houston, TX, USA.

出版信息

J Immunol Res. 2017;2017:3432701. doi: 10.1155/2017/3432701. Epub 2017 Aug 1.

DOI:10.1155/2017/3432701
PMID:28835901
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5556605/
Abstract

One of the unmet needs for asthma management is a new therapeutic agent with both anti-inflammatory and anti-smooth muscle (ASM) remodeling effects. The mannose receptor (MR) family plays an important role in allergen uptake and processing of major allergens Der p 1 and Fel d 1. We have previously reported that ASM cells express a mannose receptor (ASM-MR) and that mannan derived from (SC-MN) inhibits mannosyl-rich lysosomal hydrolase-induced bovine ASM cell proliferation. Using a humanized transgenic mouse strain (huASM-MRC2) expressing the human MRC2 receptor in a SM tissue-specific manner, we have demonstrated that ASM hyperplasia/hypertrophy can occur as early as 15 days after allergen challenge in this mouse model and this phenomenon is preventable with SC-MN treatment. This proof-of-concept study would facilitate future development of a potential asthma therapeutic agent with dual function of anti-inflammatory and anti-smooth muscle remodeling effects.

摘要

哮喘管理中未满足的需求之一是一种新的治疗剂,它具有抗炎和抗平滑肌(ASM)重塑作用。甘露糖受体(MR)家族在过敏原摄取和主要过敏原 Der p 1 和 Fel d 1 的加工中发挥重要作用。我们之前报道过,ASM 细胞表达甘露糖受体(ASM-MR),并且来源于(SC-MN)的甘露聚糖抑制富含甘露糖的溶酶体水解酶诱导的牛 ASM 细胞增殖。使用在 SM 组织特异性方式中表达人 MRC2 受体的人源化转基因小鼠品系(huASM-MRC2),我们已经证明在这种小鼠模型中,过敏原挑战后 15 天即可发生 ASM 增生/肥大,并且可以通过 SC-MN 治疗预防这种现象。这项概念验证研究将促进具有抗炎和抗平滑肌重塑作用的潜在哮喘治疗剂的未来发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/16a7d1082062/JIR2017-3432701.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/1d9f682ed2af/JIR2017-3432701.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/c61ea82481d8/JIR2017-3432701.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/203a3623962d/JIR2017-3432701.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/819aecbed991/JIR2017-3432701.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/7bc861df0b08/JIR2017-3432701.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/cf89f74c49b0/JIR2017-3432701.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/8baf35bc67a3/JIR2017-3432701.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/3f4f75b8df40/JIR2017-3432701.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/16a7d1082062/JIR2017-3432701.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/1d9f682ed2af/JIR2017-3432701.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/c61ea82481d8/JIR2017-3432701.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/203a3623962d/JIR2017-3432701.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/819aecbed991/JIR2017-3432701.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/7bc861df0b08/JIR2017-3432701.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/cf89f74c49b0/JIR2017-3432701.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/8baf35bc67a3/JIR2017-3432701.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/3f4f75b8df40/JIR2017-3432701.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82f6/5556605/16a7d1082062/JIR2017-3432701.009.jpg

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