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首页> 外文期刊>Annals of the New York Academy of Sciences >Lack of Dendritic Cell Maturation Following Infection by Coxiella burnetii Synthesizing Different Lipopolysaccharide Chemotypes
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Lack of Dendritic Cell Maturation Following Infection by Coxiella burnetii Synthesizing Different Lipopolysaccharide Chemotypes

机译:柯氏杆菌感染后树突状细胞成熟的缺乏合成不同的脂多糖化学型。

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Coxiella burnetii is an obligate intracellular bacterium and the etio-logic agent of the zoonotic disease Q fever. Symptomatic infection is normally characterized by flu-like symptoms; however, in some cases, a persistent infection can ensue that may reactivate months or years after initial exposure to cause chronic disease. The mechanisms by which this obligate parasite evades clearance by the host immune response during persistent infection are unknown. We have previously demonstrated that lipopolysaccharide (LPS) length is critical in determining the response of human dendritic cells (DC) to C. burnetii. Here, we investigated whether LPS chemotype affects DC maturation or activation. Immature human DC were infected with three virulent strains of C. burnetii (Nine Mile phase Ⅰ, S, or Priscilla) that produce chemically distinct LPS molecules. None of these strains stimulated significant upregulation of cell surface markers of DC maturation. Moreover, these strains were equally deficient in inducing DC IL-12p70 production or p38 mitogen-activated protein kinase phosphorylation. Infection of DC by virulent C. burnetii without stimulating significant maturation or inflammatory cytokine production may be a mechanism of immune evasion that results in persistent infection of an otherwise immuno-competent host. Our data indicate that LPS chemotype is not a determinant of DC maturation or cytokine production in response to C. burnetii.
机译:伯氏柯氏杆菌是专性细胞内细菌,是人畜共患病Q发热的病原体。有症状的感染通常以流感样症状为特征。但是,在某些情况下,可能会发生持续性感染,这种感染可能会在初次接触后数月或数年重新激活,从而引起慢性疾病。在持续感染过程中,这种专性寄生虫通过宿主免疫反应逃避清除的机制尚不清楚。先前我们已经证明,脂多糖(LPS)的长度对于确定人树突状细胞(DC)对伯氏梭菌的反应至关重要。在这里,我们调查了LPS的化学型是否会影响DC的成熟或激活。未成熟的人类DC感染了三株强毒的伯氏梭状芽胞杆菌菌株(九英里Ⅰ,S或Priscilla),它们产生了化学上不同的LPS分子。这些菌株均未刺激DC成熟的细胞表面标志物显着上调。此外,这些菌株在诱导DC IL-12p70产生或p38丝裂原活化的蛋白激酶磷酸化方面同样缺乏。在没有刺激显着成熟或炎性细胞因子产生的情况下,强力伯氏梭状芽胞杆菌感染DC可能是逃避免疫的机制,导致持续感染原本具有免疫能力的宿主。我们的数据表明,LPS的化学型不是决定DC成熟或细胞因子生成对伯氏梭菌的反应的决定因素。

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