“防御素”是先天免疫系統(tǒng)的關(guān)鍵“效應(yīng)子”分子,，保護(hù)宿主不受感染性微生物侵害并決定粘膜表面上微生物群的組成,。“人β-防御素-1” (hBD-1)是同類中最著名的肽之一,，由幾乎所有的人上皮點(diǎn)表達(dá)，但以前的研究工作表明,，它與其他“防御素”相比抗菌活性低?，F(xiàn)在,，Jan Wehkamp及其同事發(fā)現(xiàn)，在與結(jié)腸末端相似的還原條件下,，hBD-1表現(xiàn)出針對潛在病原體白色念珠菌,、雙岐桿菌和乳酸菌的強(qiáng)力抗菌性。試管實(shí)驗(yàn)證據(jù)表明,，“硫氧還蛋白”是最有可能掩蔽hBD-1在小腸上皮中抗菌活性的還原劑,。（生物谷Bioon.com）
生物谷推薦原文出處：
Nature doi:10.1038/nature09674
Reduction of disulphide bonds unmasks potent antimicrobial activity of human β-defensin 1
Bjoern O. Schroeder,Zhihong Wu,Sabine Nuding,Sandra Groscurth,Moritz Marcinowski,Julia Beisner,Johannes Buchner,Martin Schaller,Eduard F. Stange& Jan Wehkamp
Human epithelia are permanently challenged by bacteria and fungi, including commensal and pathogenic microbiota1, 2. In the gut, the fraction of strict anaerobes increases from proximal to distal, reaching 99% of bacterial species in the colon3. At colonic mucosa, oxygen partial pressure is below 25% of airborne oxygen content, moreover microbial metabolism causes reduction to a low redox potential of ?200?mV to –300?mV in the colon4. Defensins, characterized by three intramolecular disulphide-bridges, are key effector molecules of innate immunity that protect the host from infectious microbes and shape the composition of microbiota at mucosal surfaces5, 6, 7, 8. Human β-defensin 1 (hBD-1) is one of the most prominent peptides of its class but despite ubiquitous expression by all human epithelia, comparison with other defensins suggested only minor antibiotic killing activity9, 10. Whereas much is known about the activity of antimicrobial peptides in aerobic environments, data about reducing environments are limited. Herein we show that after reduction of disulphide-bridges hBD-1 becomes a potent antimicrobial peptide against the opportunistic pathogenic fungus Candida albicans and against anaerobic, Gram-positive commensals of Bifidobacterium and Lactobacillus species. Reduced hBD-1 differs structurally from oxidized hBD-1 and free cysteines in the carboxy terminus seem important for the bactericidal effect. In vitro, the thioredoxin (TRX) system11 is able to reduce hBD-1 and TRX co-localizes with reduced hBD-1 in human epithelia. Hence our study indicates that reduced hBD-1 shields the healthy epithelium against colonisation by commensal bacteria and opportunistic fungi. Accordingly, an intimate interplay between redox-regulation and innate immune defence seems crucial for an effective barrier protecting human epithelia
