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首页> 外文期刊>Cytokine >Pathogen specific cytokine release reveals an effect of TLR2 Arg753Gln during Candida sepsis in humans.
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Pathogen specific cytokine release reveals an effect of TLR2 Arg753Gln during Candida sepsis in humans.

机译：病原体特异性细胞因子的释放揭示了人类念珠菌败血症中TLR2 Arg753Gln的作用。

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Toll-like receptors (TLRs) are crucial pattern-recognition receptors (PRRs) for activation of innate and adapted immunity. TLR2 heterodimerizes with TLR1 or TLR6 to recognize multiple pathogen-associated molecular patterns (PAMPs) of fungi, Gram-positive pathogens, and mycobacteria. Receptor activation culminates in monocyte, T-helper (Th)1, and Th2 cytokine release. Single nucleotide polymorphisms (SNPs) Arg753Gln and Arg677Trp affect TLR2 responsiveness and may contribute to the course of sepsis, which is associated with substantial morbidity and mortality during intensive care treatment. We genotyped 325 critically ill patients with septic shock, and performed a detailed clinical follow-up with 47 of these patients. Here, we investigated whether distinct sepsis episodes result in defined plasma cytokine patterns, and whether cytokine profiles may be linked to the TLR2 polymorphisms. Blood sampling was done daily and microbiological testing was performed on a routine basis. DNA was extracted from whole blood and TLR2 SNPs were typed by pyrosequencing. Cytokines were measured by multiplexed array technologies and the leukocyte phenotype was determined by flow cytometry. Among the 325 ICU patients, 17 individuals (5.2%) were heterozygous for Arg753Gln. The SNP Arg677Trp was not found in any patient. Episodes of Gram-negative, Gram-positive, and Candida sepsis were recorded. During Gram-positive sepsis, the cytokine pattern did not differ between Arg753Gln heterozygous patients and wild type patients. By contrast, during Candida sepsis, the Arg753Gln heterozygous patients showed biomarker patterns that differed from wild type patients with elevated TNF-alpha plasma concentrations, but reduced IFN-gamma and IL-8 levels. In conclusion, TLR2 SNP Arg753Gln results in altered cytokine release in response to Candida but not to Gram-positive sepsis.
机译：Toll样受体（TLR）是激活先天免疫和适应性免疫的关键模式识别受体（PRR）。 TLR2与TLR1或TLR6异源二聚体，以识别真菌，革兰氏阳性病原体和分枝杆菌的多种病原体相关分子模式（PAMP）。受体激活在单核细胞，T辅助（Th）1和Th2细胞因子释放中达到顶点。单核苷酸多态性（SNPs）Arg753Gln和Arg677Trp影响TLR2反应性，并可能导致败血症的发生，这与重症监护期间的大量发病率和死亡率有关。我们对325名败血症性休克重症患者进行了基因分型，并对其中47名患者进行了详细的临床随访。在这里，我们调查了不同的败血症发作是否导致定义的血浆细胞因子模式，以及细胞因子谱是否可能与TLR2多态性相关。每天进行血液采样，并按常规进行微生物检测。从全血中提取DNA，并通过焦磷酸测序对TLR2 SNP进行分型。通过多重阵列技术测量细胞因子，并通过流式细胞术确定白细胞表型。在325名ICU患者中，有17名（5.2％）的人是Arg753Gln的杂合子。在任何患者中均未发现SNP Arg677Trp。记录革兰氏阴性，革兰氏阳性和念珠菌败血症的发作。在革兰氏阳性脓毒症期间，Arg753Gln杂合患者和野生型患者之间的细胞因子模式没有差异。相比之下，在念珠菌败血症期间，Arg753Gln杂合患者显示出与野生型患者不同的生物标志物模式，野生型患者的TNF-α血浆浓度升高，但IFN-γ和IL-8水平降低。总之，TLR2 SNP Arg753Gln导致对念珠菌但对革兰氏阳性败血症无反应的细胞因子释放改变。

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