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抗菌肽 AMP-IBP5 通过低密度脂蛋白受体相关蛋白-1 受体抑制特应性皮炎小鼠模型中的皮炎样损伤。

The Antimicrobial Peptide AMP-IBP5 Suppresses Dermatitis-like Lesions in a Mouse Model of Atopic Dermatitis through the Low-Density Lipoprotein Receptor-Related Protein-1 Receptor.

机构信息

Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.

Department of Dermatology and Allergology, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.

出版信息

Int J Mol Sci. 2023 Mar 8;24(6):5200. doi: 10.3390/ijms24065200.

DOI:10.3390/ijms24065200
PMID:36982275
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10049508/
Abstract

The antimicrobial peptide derived from insulin-like growth factor-binding protein 5 (AMP-IBP5) exhibits antimicrobial activities and immunomodulatory functions in keratinocytes and fibroblasts. However, its role in regulating skin barrier function remains unclear. Here, we investigated the effects of AMP-IBP5 on the skin barrier and its role in the pathogenesis of atopic dermatitis (AD). 2,4-Dinitrochlorobenzene was used to induce AD-like skin inflammation. Transepithelial electrical resistance and permeability assays were used to investigate tight junction (TJ) barrier function in normal human epidermal keratinocytes and mice. AMP-IBP5 increased the expression of TJ-related proteins and their distribution along the intercellular borders. AMP-IBP5 also improved TJ barrier function through activation of the atypical protein kinase C and Rac1 pathways. In AD mice, AMP-IBP5 ameliorated dermatitis-like symptoms restored the expression of TJ-related proteins, suppressed the expression of inflammatory and pruritic cytokines, and improved skin barrier function. Interestingly, the ability of AMP-IBP5 to alleviate inflammation and improve skin barrier function in AD mice was abolished in mice treated with an antagonist of the low-density lipoprotein receptor-related protein-1 (LRP1) receptor. Collectively, these findings indicate that AMP-IBP5 may ameliorate AD-like inflammation and enhance skin barrier function through LRP1, suggesting a possible role for AMP-IBP5 in the treatment of AD.

摘要

胰岛素样生长因子结合蛋白 5 衍生的抗菌肽 (AMP-IBP5) 在角质形成细胞和成纤维细胞中具有抗菌活性和免疫调节功能。然而，其在调节皮肤屏障功能中的作用尚不清楚。在这里，我们研究了 AMP-IBP5 对皮肤屏障的影响及其在特应性皮炎 (AD) 发病机制中的作用。使用 2,4-二硝基氯苯诱导 AD 样皮肤炎症。使用跨上皮电阻和通透性测定法研究正常人类表皮角质形成细胞和小鼠中的紧密连接 (TJ) 屏障功能。AMP-IBP5 增加了 TJ 相关蛋白的表达及其在细胞间边界的分布。AMP-IBP5 还通过激活非典型蛋白激酶 C 和 Rac1 途径改善 TJ 屏障功能。在 AD 小鼠中，AMP-IBP5 改善了类似皮炎的症状，恢复了 TJ 相关蛋白的表达，抑制了炎症和瘙痒细胞因子的表达，并改善了皮肤屏障功能。有趣的是，在接受低密度脂蛋白受体相关蛋白-1 (LRP1) 受体拮抗剂治疗的小鼠中，AMP-IBP5 减轻 AD 小鼠炎症和改善皮肤屏障功能的能力被消除。综上所述，这些发现表明，AMP-IBP5 可能通过 LRP1 改善 AD 样炎症和增强皮肤屏障功能，提示 AMP-IBP5 在 AD 治疗中的可能作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d1/10049508/1c986501e513/ijms-24-05200-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d1/10049508/88709d86f676/ijms-24-05200-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d1/10049508/6b1c85dd084d/ijms-24-05200-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d1/10049508/474bbac36de7/ijms-24-05200-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d1/10049508/1c986501e513/ijms-24-05200-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d1/10049508/88709d86f676/ijms-24-05200-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d1/10049508/96f1f1eb1d6d/ijms-24-05200-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d1/10049508/5097bdb9a121/ijms-24-05200-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d1/10049508/bead3ae44120/ijms-24-05200-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32d1/10049508/6b1c85dd084d/ijms-24-05200-g007.jpg
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