Blood:在肝脏和脾脏中,沙门氏菌诱导的血栓形成不同步发生,且不能有效捕获细菌

2018-11-10 MedSci MedSci原创

中心点:沙门氏菌感染后,脾脏和肝脏中的血栓形成具有不同的动力学。肝脾血栓不是局限细菌的主要部位。摘要:血栓是一种常见的、可危及生命的全身性感染并发症,与多器官损伤相关。Nonantzin Beristain-Covarrubias等研究人员既往发现了一种由鼠伤寒沙门氏菌感染引起的炎症驱动血栓形成的新机制。肝内血栓形成发生在感染消退后的7天内,为单核细胞依赖性的。意料之外的是,虽然脾脏与肝脏有类似的

中心点:

沙门氏菌感染后,脾脏和肝脏中的血栓形成具有不同的动力学。

肝脾血栓不是局限细菌的主要部位。

摘要:

血栓是一种常见的、可危及生命的全身性感染并发症,与多器官损伤相关。Nonantzin Beristain-Covarrubias等研究人员既往发现了一种由鼠伤寒沙门氏菌感染引起的炎症驱动血栓形成的新机制。肝内血栓形成发生在感染消退后的7天内,为单核细胞依赖性的。意料之外的是,虽然脾脏与肝脏有类似的细菌负担,但此时脾脏的血栓并不明显。

在本研究中,研究人员发现血栓形成确实在脾脏内发生,但与肝脏相比血流动力学加速明显,特别是在24小时内,随后血栓被迅速分解。血栓形成的独特动力学和细菌负担提供了一种假设的检验,即血栓在健康血管中形成来捕获或清除循环中的细菌,通常称为免疫性血栓。

值得注意的是,在感染早期,虽然在被感染的脾脏和肝脏中都可检测到细菌,但组织切片的免疫组化分析显示血栓中仅含有极少量细菌。与此相反,在体外沙门氏菌诱导的血小板聚集物中,可检测到细菌。

综上所述,血栓形成具有器官动力学特异性,该结论对传统认知——免疫血栓捕获体内细菌机制的普遍性——发出挑战。


原始出处:

Nonantzin Beristain-Covarrubias,et al. Salmonella-induced thrombi in mice develop asynchronously in the spleen and liver and are not effective bacterial traps. Blood  2018  :blood-2018-08-867267;  doi: https://doi.org/10.1182/blood-2018-08-867267

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    2018-11-13 衣带渐宽

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    2018-11-12 清风拂面

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    2018-11-10 医者仁心5538

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    2018-11-10 天地飞扬

    了解一下,谢谢分享!

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一提到细菌,人们就会想起沙门氏菌、结核杆菌等很多导致疾病的罪魁祸首,但细菌也不全都是有害的,人体肠道内就有很多益生菌一直在默默守护着我们,它们可以帮助消化食物、分泌一些我们不能合成的营养素,增强我们的免疫力等。近日,斯坦福大学的科学家们还发现,肠道菌群分泌的副产物可以帮助抵御致病的沙门氏菌。