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白细胞介素-1β是否为椎间盘退变疾病中[具体内容缺失]作用的进一步证据?来自炎症性皮肤病寻常痤疮研究的经验教训。

Is IL-1β Further Evidence for the Role of in Degenerative Disc Disease? Lessons From the Study of the Inflammatory Skin Condition Acne Vulgaris.

作者信息

Slaby Ondrej, McDowell Andrew, Brüggemann Holger, Raz Assaf, Demir-Deviren Sibel, Freemont Tony, Lambert Peter, Capoor Manu N

机构信息

Central European Institute of Technology, Masaryk University, Brno, Czechia.

Northern Ireland Centre for Stratified Medicine, School of Biomedical Sciences, Ulster University, Londonderry, United Kingdom.

出版信息

Front Cell Infect Microbiol. 2018 Aug 14;8:272. doi: 10.3389/fcimb.2018.00272. eCollection 2018.

Abstract

The pathogenesis of degenerative disc disease is a complex and multifactorial process in which genetics, mechanical trauma, altered loading and nutrition present significant etiological factors. Infection of the intervertebral disc with the anaerobic bacterium is now also emerging as a potentially new etiological factor. This human commensal bacterium is well known for its long association with the inflammatory skin condition acne vulgaris. A key component of inflammatory responses to in acne appears to be interleukin (IL)-1β. Similarly, in degenerative disc disease (DDD) there is compelling evidence for the fundamental roles of IL-1β in its pathology. We therefore propose that involvement in DDD is biologically very plausible, and that IL-1β is the key inflammatory mechanism driving the host response to infection. Since there is a solid theoretical basis for this phenomenon, we further propose that the relationship between infection and DDD is causal.

摘要

椎间盘退变疾病的发病机制是一个复杂的多因素过程,其中遗传、机械创伤、负荷改变和营养状况是重要的病因因素。现在,椎间盘被厌氧菌感染也正成为一种潜在的新病因。这种人体共生细菌因长期与炎症性皮肤病寻常痤疮相关而闻名。痤疮中对白介素(IL)-1β的炎症反应的一个关键组成部分。同样,在椎间盘退变疾病(DDD)中,有令人信服的证据表明IL-1β在其病理过程中起基本作用。因此,我们认为[细菌名称]参与DDD在生物学上是非常合理的,并且IL-1β是驱动宿主对[细菌名称]感染反应的关键炎症机制。由于这种现象有坚实的理论基础,我们进一步提出[细菌名称]感染与DDD之间的关系是因果关系。 (注:原文中“anaerobic bacterium”和“this human commensal bacterium”未明确具体细菌名称,翻译时保留英文表述)

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57b2/6103242/7c63d2433071/fcimb-08-00272-g0001.jpg

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