Keratinocyte expression of human β defensin 2 following bacterial infection:: Role in cutaneous host defense
Keratinocyte expression of human β defensin 2 following bacterial infection:: Role in cutaneous host defense
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DOI：
10.1128/cdli.10.1.161-166.2003
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发表时间：
2003-01-01
期刊：
影响因子：
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通讯作者：
Darmstadt, GL
中科院分区：
文献类型：
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作者：
Dinulos, JGH;Mentele, L;Darmstadt, GL
人β防御素2（hbetaD-2）被认为在皮肤免疫防御中起重要作用。我们假设（i）通过逆转录-PCR测量的hbetaD-2的角质形成细胞表达将响应于病原菌的挑战而上调，特别是高度粘附的化脓性链球菌和金黄色葡萄球菌菌株，以及（ii）hbetaD-2将对病原体而不是微生物具有有效的抗微生物活性。hbetaD-2的表达被S.金黄色葡萄球菌、表皮葡萄球菌、大肠杆菌和铜绿假单胞菌，而S.化脓性链球菌是hbetaD-2的较差和可变的诱导剂。细菌粘附水平与hbetaD-2的角质形成细胞表达之间没有相关性。S.化脓性链球菌对hbetaD-2的杀伤作用比S.表皮。我们的结论是，诱导hbetaD-2表达的能力加上对其抗菌作用的敏感性可能导致革兰氏阴性细菌生物体皮肤感染的罕见性，而S.化脓性链球菌可能在其逃避先天防御和引起皮肤病的能力方面很重要。诱导hbetaD-2的表达，但对hbetaD-2的相对耐受可能使S.当角质层屏障被破坏时，表皮细胞存活在皮肤表面并调节hbetaD-2表达。
Human beta defensin 2 (hbetaD-2) is thought to play an important role in cutaneous immune defense. We hypothesized that (i) keratinocyte expression of hbetaD-2, measured by reverse transcription-PCR, would be upregulated in response to challenge with pathogenic bacteria, particularly highly adherent strains of Streptococcus pyogenes and Staphylococcus aureus, and (ii) hbetaD-2 would have potent antimicrobial activity against pathogenic but not commensal organisms. Expression of hbetaD-2 was induced consistently by S. aureus, Staphylococcus epidermidis, Escherichia coli, and Pseudomonas aeruginosa, whereas strains of S. pyogenes were poor and variable inducers of hbetaD-2. No correlation was found between levels of bacterial adherence and keratinocyte expression of hbetaD-2. S. pyogenes was significantly more sensitive to killing by hbetaD-2 than S. epidermidis. We conclude that the ability to induce hbetaD-2 expression in combination with sensitivity to its antimicrobial effects may contribute to the rarity of skin infections with the gram-negative bacterial organisms, whereas lack of stimulation of hbetaD-2 expression by S. pyogenes may be important in its ability to evade innate defenses and cause skin disease. Induction of expression of hbetaD-2 but relative tolerance to it may enable S. epidermidis to survive on the skin surface and modulate hbetaD-2 expression when the stratum corneum barrier is disrupted.