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Glucocorticoid-mediated induction of caveolin-1 disrupts cytoskeletal organization, inhibits cell migration and re-epithelialization of non-healing wounds.糖皮质激素介导的小窝蛋白-1诱导破坏细胞骨架组织，抑制非愈合性伤口的细胞迁移和再上皮化。
Commun Biol. 2021 Jun 18;4(1):757. doi: 10.1038/s42003-021-02298-5.
2
MPEG1/Perforin-2 Haploinsufficiency Associated Polymicrobial Skin Infections and Considerations for Interferon-γ Therapy.MPEG1/Perforin-2 单倍体不足相关的多微生物皮肤感染和干扰素-γ 治疗的考虑因素。
Front Immunol. 2020 Nov 3;11:601584. doi: 10.3389/fimmu.2020.601584. eCollection 2020.
3
Boosts Innate Immune Response by Activation of Gamma Delta T Cells and Induction of Perforin-2 in Human Skin.通过激活γδ T细胞和诱导人皮肤中的穿孔素-2增强先天免疫反应。
Front Immunol. 2020 Sep 16;11:550946. doi: 10.3389/fimmu.2020.550946. eCollection 2020.
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Deregulated immune cell recruitment orchestrated by FOXM1 impairs human diabetic wound healing.由FOXM1精心编排的免疫细胞募集失调会损害人类糖尿病伤口愈合。
Nat Commun. 2020 Sep 16;11(1):4678. doi: 10.1038/s41467-020-18276-0.
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Maternal- and Fetal-Encoded Perforin-2 Limits Placental Infection by a Bloodborne Pathogen.母胎编码穿孔素-2 限制血源性病原体感染胎盘。
J Immunol. 2020 Oct 1;205(7):1878-1885. doi: 10.4049/jimmunol.2000615. Epub 2020 Aug 24.
6
Caspase-1 initiates apoptosis in the absence of gasdermin D.半胱氨酸天冬氨酸蛋白酶-1 在没有天冬氨酸半胱氨酸酶 D 的情况下启动细胞凋亡。
Nat Commun. 2019 May 7;10(1):2091. doi: 10.1038/s41467-019-09753-2.
7
Strain- and Species-Level Variation in the Microbiome of Diabetic Wounds Is Associated with Clinical Outcomes and Therapeutic Efficacy.糖尿病创面的微生物组在菌株和物种水平上的变化与临床结局和治疗效果相关。
Cell Host Microbe. 2019 May 8;25(5):641-655.e5. doi: 10.1016/j.chom.2019.03.006. Epub 2019 Apr 18.
8
Single cell analyses reveal specific distribution of anti-bacterial molecule Perforin-2 in human skin and its modulation by wounding and Staphylococcus aureus infection.单细胞分析揭示了抗菌分子穿孔素-2在人类皮肤中的特定分布，以及其在创伤和金黄色葡萄球菌感染时的调节作用。
Exp Dermatol. 2019 Mar;28(3):225-232. doi: 10.1111/exd.13870. Epub 2019 Feb 12.
9
Lipid Peroxidation Drives Gasdermin D-Mediated Pyroptosis in Lethal Polymicrobial Sepsis.脂质过氧化作用驱动致死性多微生物脓毒症中 GSDMD 介导的细胞焦亡。
Cell Host Microbe. 2018 Jul 11;24(1):97-108.e4. doi: 10.1016/j.chom.2018.05.009. Epub 2018 Jun 21.
10
Staphylococcus aureus Triggers Induction of miR-15B-5P to Diminish DNA Repair and Deregulate Inflammatory Response in Diabetic Foot Ulcers.金黄色葡萄球菌触发 miR-15B-5P 的诱导，以减少糖尿病足溃疡中的 DNA 修复并使炎症反应失调。
J Invest Dermatol. 2018 May;138(5):1187-1196. doi: 10.1016/j.jid.2017.11.038. Epub 2017 Dec 19.

金黄色葡萄球菌在细胞内引发细胞焦亡，并通过抑制穿孔素 2 导致愈合受到抑制。

Intracellular Staphylococcus aureus triggers pyroptosis and contributes to inhibition of healing due to perforin-2 suppression.

机构信息

Wound Healing and Regenerative Medicine Research Program, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery.

Department of Microbiology and Immunology, and.

出版信息

J Clin Invest. 2021 Dec 15;131(24). doi: 10.1172/JCI133727.

DOI:10.1172/JCI133727
PMID:34730110
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8670843/
Abstract

Impaired wound healing associated with recurrent Staphylococcus aureus infection and unresolved inflammation are hallmarks of nonhealing diabetic foot ulcers (DFUs). Perforin-2, an innate immunity molecule against intracellular bacteria, limits cutaneous infection and dissemination of S. aureus in mice. Here, we report the intracellular accumulation of S. aureus in the epidermis of DFUs with no clinical signs of infection due to marked suppression of perforin-2. S. aureus residing within the epidermis of DFUs triggers AIM2 inflammasome activation and pyroptosis. These findings were corroborated in mice lacking perforin-2. The effects of pyroptosis on DFU clinical outcomes were further elucidated in a 4-week longitudinal clinical study in patients with DFUs receiving standard care. Increased AIM2 inflammasome and ASC-pyroptosome coupled with induction of IL-1β were found in nonhealing DFUs compared with healing DFUs. Our findings revealed that perforin-2 suppression, intracellular S. aureus accumulation, and associated induction of pyroptosis contribute to healing inhibition and prolonged inflammation in patients with DFUs.

摘要

与复发性金黄色葡萄球菌感染和未解决的炎症相关的伤口愈合受损是糖尿病足溃疡（DFU）不愈合的特征。穿孔素-2 是一种针对细胞内细菌的先天免疫分子，可限制金黄色葡萄球菌在小鼠中的皮肤感染和传播。在这里，我们报告了由于穿孔素-2 的显著抑制，DFU 表皮中金黄色葡萄球菌的细胞内积累，尽管没有感染的临床迹象。DFU 表皮内存在的金黄色葡萄球菌引发 AIM2 炎性体激活和细胞焦亡。在缺乏穿孔素-2 的小鼠中证实了这些发现。在接受标准护理的 DFU 患者中进行的为期 4 周的纵向临床研究进一步阐明了细胞焦亡对 DFU 临床结局的影响。与愈合的 DFU 相比，非愈合的 DFU 中发现 AIM2 炎性体和 ASC-细胞焦亡体增加，以及 IL-1β 的诱导。我们的研究结果表明，穿孔素-2 抑制、细胞内金黄色葡萄球菌积累以及相关的细胞焦亡诱导导致 DFU 患者的愈合抑制和炎症持续时间延长。