Suppr超能文献

金黄色葡萄球菌皮肤感染的严重程度与人类β防御素 3 的诱导性有关,但与人类β防御素 2 无关。

Severity of Staphylococcus aureus infection of the skin is associated with inducibility of human beta-defensin 3 but not human beta-defensin 2.

机构信息

Institut für Tropenmedizin, Eberhard Karls Universität, Tübingen, Germany.

出版信息

Infect Immun. 2010 Jul;78(7):3112-7. doi: 10.1128/IAI.00078-10. Epub 2010 Apr 19.

Abstract

Gram-positive bacteria are the predominant cause of skin infections. Antimicrobial peptides (AMPs) are believed to be of major importance in skin's innate defense against these pathogens. This study aimed at providing clinical evidence for the contribution of AMP inducibility to determining the severity of Gram-positive skin infection. Using real-time PCR, we determined the induction of human beta-defensin 2 (HBD-2), HBD-3, and RNase 7 by comparing healthy and lesional mRNA levels in 32 patients with Gram-positive skin infection. We then examined whether AMP induction differed by disease severity, as measured by number of recurrences and need for surgical drainage in patients with Staphylococcus aureus-positive lesions. We found that HBD-2 and -3, but not RNase 7, mRNA expression was highly induced by Gram-positive bacterial infection in otherwise healthy skin. Less induction of HBD-3, but not HBD-2, was associated with more-severe S. aureus skin infection: HBD-3 mRNA levels were 11.4 times lower in patients with more than 6 recurrences (P = 0.01) and 8.8 times lower in patients reporting surgical drainage (P = 0.01) than in the respective baseline groups. This suggests that inducibility of HBD-3 influences the severity of Gram-positive skin infection in vivo. The physiological function of HBD-2 induction in this context remains unclear.

摘要

革兰氏阳性菌是皮肤感染的主要原因。抗菌肽(AMPs)被认为在皮肤先天防御这些病原体方面具有重要作用。本研究旨在为 AMP 诱导在确定革兰氏阳性皮肤感染严重程度方面的作用提供临床证据。通过实时 PCR,我们通过比较 32 名革兰氏阳性皮肤感染患者的健康和病变部位的 mRNA 水平,确定了人β防御素 2(HBD-2)、HBD-3 和 RNase 7 的诱导。然后,我们检查了 AMP 诱导是否因疾病严重程度而不同,这是通过 S. aureus 阳性病变患者的复发次数和手术引流的需要来衡量的。我们发现,HBD-2 和 -3,但不是 RNase 7,在健康皮肤的革兰氏阳性细菌感染下被高度诱导。HBD-3 的诱导减少,但不是 HBD-2,与更严重的金黄色葡萄球菌皮肤感染相关:在复发次数超过 6 次的患者中(P=0.01)和报告手术引流的患者中(P=0.01),HBD-3 的 mRNA 水平分别低 11.4 倍和 8.8 倍,与各自的基线组相比。这表明 HBD-3 的诱导可影响体内革兰氏阳性皮肤感染的严重程度。在这种情况下,HBD-2 诱导的生理功能尚不清楚。

相似文献

3
Defective killing of Staphylococcus aureus in atopic dermatitis is associated with reduced mobilization of human beta-defensin-3.
J Allergy Clin Immunol. 2008 Jul;122(1):62-8. doi: 10.1016/j.jaci.2008.04.022. Epub 2008 Jun 5.
4
Osteoblasts participate in the innate immunity of the bone by producing human beta defensin-3.
Histochem Cell Biol. 2009 Feb;131(2):207-18. doi: 10.1007/s00418-008-0522-8. Epub 2008 Oct 17.
6
IL-17 in atopic eczema: linking allergen-specific adaptive and microbial-triggered innate immune response.
J Allergy Clin Immunol. 2009 Jan;123(1):59-66.e4. doi: 10.1016/j.jaci.2008.10.031. Epub 2008 Dec 3.
7
Sebum free fatty acids enhance the innate immune defense of human sebocytes by upregulating beta-defensin-2 expression.
J Invest Dermatol. 2010 Apr;130(4):985-94. doi: 10.1038/jid.2009.384. Epub 2009 Dec 24.
9
Hepatocytes express the antimicrobial peptide HBD-2 after multiple trauma: an experimental study in human and mice.
BMC Musculoskelet Disord. 2017 Mar 7;18(1):100. doi: 10.1186/s12891-017-1458-8.

引用本文的文献

3
A Metatranscriptomics Survey of Microbial Diversity on Surfaces Post-Intervention of cleanSURFACES® Technology in an Intensive Care Unit.
Front Cell Infect Microbiol. 2021 Jul 20;11:705593. doi: 10.3389/fcimb.2021.705593. eCollection 2021.
4
Human Defensins: A Novel Approach in the Fight against Skin Colonizing a.
Antibiotics (Basel). 2020 Apr 21;9(4):198. doi: 10.3390/antibiotics9040198.
6
Immune and Inflammatory Reponses to Skin Infections.
Curr Dermatol Rep. 2018 Dec;7(4):338-349. doi: 10.1007/s13671-018-0235-8. Epub 2018 Sep 22.
7
Antimicrobial and Chemotactic Activity of Scorpion-Derived Peptide, ToAP2, against .
Toxins (Basel). 2018 May 30;10(6):219. doi: 10.3390/toxins10060219.
8
Cutaneous Nod2 Expression Regulates the Skin Microbiome and Wound Healing in a Murine Model.
J Invest Dermatol. 2017 Nov;137(11):2427-2436. doi: 10.1016/j.jid.2017.05.029. Epub 2017 Jun 22.
10
IL-22 derived from γδ T cells restricts Staphylococcus aureus infection of mechanically injured skin.
J Allergy Clin Immunol. 2016 Oct;138(4):1098-1107.e3. doi: 10.1016/j.jaci.2016.07.001. Epub 2016 Jul 15.

本文引用的文献

3
Defective killing of Staphylococcus aureus in atopic dermatitis is associated with reduced mobilization of human beta-defensin-3.
J Allergy Clin Immunol. 2008 Jul;122(1):62-8. doi: 10.1016/j.jaci.2008.04.022. Epub 2008 Jun 5.
4
Microanalysis of an antimicrobial peptide, beta-defensin-2, in the stratum corneum from patients with atopic dermatitis.
Br J Dermatol. 2008 Jul;159(1):97-104. doi: 10.1111/j.1365-2133.2008.08613.x. Epub 2008 Jul 1.
6
Management of common bacterial infections of the skin.
Curr Opin Infect Dis. 2008 Apr;21(2):122-8. doi: 10.1097/QCO.0b013e3282f44c63.
7
Antimicrobial peptides in human skin disease.
Eur J Dermatol. 2008 Jan-Feb;18(1):11-21. doi: 10.1684/ejd.2008.0304. Epub 2007 Dec 18.
8
Expression of antimicrobial peptides in the normal and involved skin of patients with infective cellulitis.
J Infect Dis. 2007 Nov 1;196(9):1425-30. doi: 10.1086/522630. Epub 2007 Sep 27.
9
The constitutive capacity of human keratinocytes to kill Staphylococcus aureus is dependent on beta-defensin 3.
J Invest Dermatol. 2007 Oct;127(10):2368-80. doi: 10.1038/sj.jid.5700861. Epub 2007 Apr 26.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验