Cell Res:黄波团队揭秘新冠患者早期沉默式乏氧的原因

2020-11-21 Bio生物世界 Bio生物世界

新冠病毒SARS-CoV-2传播所致全球大流行迄今仍未见消退迹象,但已导致5000多万民众被感染,超过130万人死于新冠,目前依然没有治疗和预防新冠感染的有效药物。

新冠病毒SARS-CoV-2传播所致全球大流行迄今仍未见消退迹象,但已导致5000多万民众被感染,超过130万人死于新冠,目前依然没有治疗和预防新冠感染的有效药物。不管国际上对新冠病毒的紧迫研究,新冠病毒感染真正的发病机理仍然不清,特别是病毒感染早期的关键性细胞和分子事件未被揭示,成为破解新冠难题的重要制约因素。

中国医学科学院基础医学研究所黄波团队在 Cell Research 在线发表了题为:Mucus production by IFN-AhR signaling triggers hypoxia of COVID-19 patients 的研究论文,解开了新冠致病早期的关键环节。

肺的功能是吸入氧气和排出二氧化碳,这种气体的流动发生在呼吸道,主要通过气管、支气管和细小支气管来完成的,但在吸入气体时,不可避免地将外源性细菌和病毒吸入,为了防御这种病原菌的入侵,呼吸道部位进化出一套分泌粘液的机制,该粘液覆盖于气道表面,通过粘附住细小微生物,阻止它们感染细胞。

同时,气管、支气管和细小支气管表面有大量的纤毛,其向上摆动,可将粘附有病原菌的粘液排出至咽喉部位,以痰液的形式排出体外,从而维护肺的洁净。空气经过气管和支气管最后会进入细小支气管末端膨胀如气球样的部位,称之为肺泡,并在肺泡进行氧气和二氧化碳交换,即氧气穿过肺泡壁及与肺泡壁相依的毛细血管壁而进入血液,而血液中二氧化碳则穿过血管壁和肺泡壁而进入肺泡,通过呼气而被排出。不同于气管和支气管,肺泡不产生粘液,表面也没有纤毛,从而维持肺泡干燥,便于气体交换,但肺泡表面有薄薄一层液体,形成表面张力以维持肺部的伸张结构。

黄波团队研究发现,新冠病毒感染时,病毒入侵肺泡部位导致II型肺泡上皮细胞分泌粘液,后者沉积于肺泡表面,增加了肺泡部位气体穿过的屏障,导致最早期的机体缺氧。在机制上,团队研究发现,SARS-CoV-2感染并不直接诱导被感染的细胞产生粘液,而是通过刺激免疫细胞所释放的干扰素而引发的。黄波团队证实,干扰素通过IDO-Kyn分子信号途径,最终激活关键性转录因子AhR,后者直接诱导黏蛋白基因的表达,使得肺泡上皮细胞分泌粘液。干扰素作为抗病毒感染的核心因子,这种诱发粘液的作用,依然是对细胞的保护,但却启动了肺组织的病理改变,实乃“好心办坏事”。

这项研究解开了临床“silent hypoxia (沉默式乏氧)”之谜。临床观察发现,很多新冠病人早期并没有出现症状,而乏氧已产生,其血氧饱和度可低至60%,这种早期神秘的乏氧形成,因不清楚其背后机理,国外临床界称之为“silent hypoxia”。机体对于乏氧其实有很好的耐受性,但对于体内CO2堆积则不耐受。原因有两点:一是血中CO2含量增加会导致机体酸中毒;更重要的一点是,CO2是能量生成过程中三羧酸循环的产物,其堆积妨碍能量代谢和生成。但早期分泌的粘液在肺泡部位仅对O2产生影响,而对CO2没有影响?这是由于CO2的溶解度是O2的20倍以上,故只有当肺泡部位沉积的粘液量达到一定程度,才会妨碍CO2离开血液和进入肺泡。

这项研究对于新冠病毒感染提供了潜在治疗策略。尽管新冠病毒传染性非常强,但大多数被感染者,并未出现明显症状或者症状较轻,提示机体免疫系统能够很好地控制病毒。对于重症患者而言,如果能够在早期阶段减缓肺功能的损害,为机体特异性抗病毒免疫(T细胞和B细胞应答)的形成赢得时间,则有可能阻止病情向重症转变,或者阻止重症向死亡发展。考虑到SARS、MERS、Ebola病毒和新冠病毒致病的相似性,这项研究对于SARS、MERS和Ebola病毒感染的防治也具有借鉴意义。

原始出处:

Yuying Liu, Jiadi Lv, Jiangning Liu, et al.Mucus production stimulated by IFN-AhR signaling triggers hypoxia of COVID-19.Cell Res. 2020 Nov 6;1-10. doi: 10.1038/s41422-020-00435-z.

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    2021-03-28 维他命
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    2020-11-22 蛮小吉

    0

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    2020-11-21 公卫新人

    新冠肺炎,疫情何时才能消失

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    2020-11-21 1def5843m65(暂无匿称)

    那么是否应该对武汉疫情中使用干扰素的患者进行大规模的回顾性的研究?

    0

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