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Adrenal Steroids Modulate the Immune Response during Brucella abortus Infection by a Mechanism That Depends on the Regulation of Cytokine Production

机译:肾上腺类固醇通过依赖细胞因子生产的调节机制调节布鲁氏菌流产感染期间的免疫反应。

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Human brucellosis is a protean disease with a diversity of clinical signs and symptoms resulting from infection with Brucella species. Recent reports suggest a cross-regulation between adrenal steroids (cortisol and dehydroepiandrosterone [DHEA]) and the immune system. Monocytes and macrophages are the main replication niche for Brucella. Therefore, we investigated the role of adrenal hormones on the modulation of the immune response mediated by macrophages in B. abortus infection. Cortisol treatment during B. abortus infection significantly inhibits cytokine, chemokine, and MMP-9 secretion. In contrast, DHEA treatment had no effect. However, DHEA treatment increases the expression of costimulatory molecules (CD40, CD86), the adhesion molecule CD54, and major histocompatibility complex class I (MHC-I) and MHC-II expression on the surface of B. abortus-infected monocytes. It is known that B. abortus infection inhibits MHC-I and MHC-II expression induced by gamma interferon (IFN-γ) treatment. DHEA reverses B. abortus downmodulation of the MHC-I and -II expression induced by IFN-γ. Taken together, our data indicate that DHEA immune intervention may positively affect monocyte activity during B. abortus infection.
机译:人类布鲁氏菌病是一种蛋白质病,由布鲁氏菌属感染引起,具有多种临床体征和症状。最近的报道表明肾上腺类固醇(皮质醇和脱氢表雄酮[DHEA])与免疫系统之间存在交叉调节。单核细胞和巨噬细胞是布鲁氏菌的主要复制位。因此,我们研究了肾上腺激素在流产双歧杆菌感染中由巨噬细胞介导的免疫应答调节中的作用。流产双歧杆菌感染期间的皮质醇治疗可显着抑制细胞因子,趋化因子和MMP-9的分泌。相反,DHEA治疗没有效果。但是,DHEA治疗会增加流产双歧杆菌感染的单核细胞表面上的共刺激分子(CD40,CD86),粘附分子CD54以及主要组织相容性复合体I类(MHC-I)和MHC-II的表达。已知流产芽孢杆菌感染抑制了γ-干扰素(IFN-γ)治疗诱导的MHC-1和MHC-II表达。 DHEA逆转了IFN-γ诱导的流产芽孢杆菌对MHC-1和-II表达的下调。两者合计,我们的数据表明DHEA免疫干预可能会积极影响B.流产感染过程中的单核细胞活性。

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