IL-4/IL-13 remodeling pathway of COVID-19 lung injury.
IL-4/IL-13 remodeling pathway of COVID-19 lung injury.
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DOI：
10.1038/s41598-020-75659-5
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发表时间：
2020-10-29
影响因子：
4.6
通讯作者：
de Noronha L
中科院分区：
文献类型：
--
作者：
Vaz de Paula CB;de Azevedo MLV;Nagashima S;Martins APC;Malaquias MAS;Miggiolaro AFRDS;da Silva Motta Júnior J;Avelino G;do Carmo LAP;Carstens LB;de Noronha L
与H1N1 pdm 09（大流行性甲型流感病毒H1N1亚型）相比，COVID-19的致死率很高，尽管两者都会导致炎症反应加重，但两种大流行性肺炎的机制差异需要澄清。因此，我们的目标是分析死于COVID-19的患者中白细胞介素4、13（IL-4、IL-13）、转化生长因子-β（TGF-β）和M2巨噬细胞（鞘氨醇-1）的组织表达，并与H1N1 pdm 09引起的严重肺病病例和无肺损伤的对照组进行比较。使用了6例死于SARS-CoV-2的患者（COVID-19组）的肺活检样本，并与10例死于H1N1 pdm 09严重感染的成人（H1N1组）和11例死于不同原因而无肺损伤的患者（对照组）的肺样本进行了比较。免疫组化法检测IL-4、IL-13、TGF-β的表达及M2巨噬细胞评分（鞘氨醇-1）。与H1N1和对照组相比，在COVID-19组中观察到M2巨噬细胞中的IL-4组织表达和鞘氨醇-1显著更高。观察到SARS-CoV-2与H1N1 pdm 09感染的弥漫性肺泡损伤（DAD）的不同机制。IL-4表达和肺重塑是在SARS-CoV-2和H1N1 pdm 09中观察到的现象。然而，SARS-CoV-2似乎通过不同的机制促进肺损伤，如Th 1/Th 17反应的参与不足和Th 2的参与较高。理解和管理由SARS-CoV-2引起的加重和无效的免疫应答需要进一步澄清以改进治疗方案。
The COVID-19 fatality rate is high when compared to the H1N1pdm09 (pandemic Influenza A virus H1N1 subtype) rate, and although both cause an aggravated inflammatory response, the differences in the mechanisms of both pandemic pneumonias need clarification. Thus, our goal was to analyze tissue expression of interleukins 4, 13, (IL-4, IL-13), transforming growth factor-beta (TGF-β), and the number of M2 macrophages (Sphingosine-1) in patients who died by COVID-19, comparing with cases of severe pneumopathy caused by H1N1pdm09, and a control group without lung injury. Six lung biopsy samples of patients who died of SARS-CoV-2 (COVID-19 group) were used and compared with ten lung samples of adults who died from a severe infection of H1N1pdm09 (H1N1 group) and eleven samples of patients who died from different causes without lung injury (CONTROL group). The expression of IL-4, IL-13, TGF-β, and M2 macrophages score (Sphingosine-1) were identified through immunohistochemistry (IHC). Significantly higher IL-4 tissue expression and Sphingosine-1 in M2 macrophages were observed in the COVID-19 group compared to both the H1N1 and the CONTROL groups. A different mechanism of diffuse alveolar damage (DAD) in SARS-CoV-2 compared to H1N1pdm09 infections were observed. IL-4 expression and lung remodeling are phenomena observed in both SARS-CoV-2 and H1N1pdm09. However, SARS-CoV-2 seems to promote lung damage through different mechanisms, such as the scarce participation Th1/Th17 response and the higher participation of the Th2. Understanding and managing the aggravated and ineffective immune response elicited by SARS-CoV-2 merits further clarification to improve treatments propose.
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