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首页> 外文期刊>Infection and immunity >Innate Immune Response of Oral and Foreskin Keratinocytes: Utilization of Different Signaling Pathways by Various Bacterial Species
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Innate Immune Response of Oral and Foreskin Keratinocytes: Utilization of Different Signaling Pathways by Various Bacterial Species

机译：口腔和包皮角质形成细胞的先天免疫反应：不同细菌物种对不同信号通路的利用

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The innate immune response is critical for the epithelial antimicrobial barrier. The human β-defensins are small, cationic antimicrobial peptides that are made by epithelial cells and that play a role in mucosal and skin defenses. Human β-defensin 1 (hBD-1) is expressed constitutively in epithelial tissues, whereas hBD-2 and hBD-3 are expressed in response to bacterial stimuli or inflammation. Previous studies showed that hBD-2 was induced by Fusobacterium nucleatum cell wall extract without the involvement of the NF-κB transcription factors, which typically are associated with innate immunity and inflammation. The goal of this study was to characterize signaling pathways involved in hBD-2 induction in response to commensal and pathogenic bacteria. Cultured human oral and foreskin keratinocytes were treated separately with inhibitors of NF-κB, c-Jun N-terminal kinase (JNK), and p38 and then stimulated with oral commensal Streptococcus gordonii, oral pathogens Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, skin commensal Staphylococcus epidermidis, or skin pathogen Streptococcus pyogenes. Different bacteria induced different levels of hBD-2 and in response to the various inhibitors tested, although certain common patterns were observed for commensal- and pathogen-stimulated cells. hBD-2 induction by all bacteria tested was partially or completely blocked by inhibitors of the JNK and p38 pathways. However, in addition, hBD-2 induction by pathogenic bacteria in both oral and foreskin keratinocytes was blocked by inhibitors of NF-κB. The results indicate that commensal and pathogenic bacteria utilize different pathways in hBD-2 induction and suggest that epithelial cells from different body sites have common signaling mechanisms to distinguish between commensal and pathogenic bacteria.
机译：先天性免疫应答对于上皮抗微生物屏障至关重要。人β-防御素是由上皮细胞制成的小阳离子抗微生物肽，在粘膜和皮肤防御中起作用。人β-防御素1（hBD-1）在上皮组织中组成性表达，而hBD-2和hBD-3在对细菌刺激或炎症反应中表达。先前的研究表明，hBD-2是由细胞壁提取物诱导的，而没有涉及通常与先天免疫和炎症相关的NF-κB转录因子。这项研究的目的是表征响应共生细菌和病原细菌而参与hBD-2诱导的信号通路。将培养的人口腔和包皮角质形成细胞分别用NF-κB，c-Jun N末端激酶（JNK）和p38抑制剂处理，然后用口服共生菌戈登链球菌刺激，口服病原体牙龈卟啉菌和放线放线放线杆菌，皮肤常见表皮葡萄球菌或皮肤病原体化脓性链球菌。尽管观察到了经共刺激和病原体刺激的细胞，某些细菌观察到了某些共同的模式，但不同的细菌诱导了不同水平的hBD-2并响应测试的各种抑制剂。 JNK和p38途径的抑制剂部分或完全阻断了所有测试细菌对hBD-2的诱导。但是，此外，在口腔和包皮角质形成细胞中，致病菌对hBD-2的诱导被NF-κB抑制剂阻断。结果表明，共生和致病菌在hBD-2诱导中采用不同的途径，并表明来自不同身体部位的上皮细胞具有共同的信号传导机制来区分共生和致病菌。

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