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The role of the lectin pathway of the complement system in SARS-CoV-2 lung injury.补体系统凝集素途径在 SARS-CoV-2 肺损伤中的作用。
Transl Res. 2021 May;231:55-63. doi: 10.1016/j.trsl.2020.11.008. Epub 2020 Nov 20.
2
IL-4/IL-13 remodeling pathway of COVID-19 lung injury.新冠肺炎肺损伤的 IL-4/IL-13 重塑途径。
Sci Rep. 2020 Oct 29;10(1):18689. doi: 10.1038/s41598-020-75659-5.
3
Mast Cells in Alveolar Septa of COVID-19 Patients: A Pathogenic Pathway That May Link Interstitial Edema to Immunothrombosis.COVID-19 患者肺泡隔中的肥大细胞:一种可能将间质水肿与免疫血栓联系起来的致病途径。
Front Immunol. 2020 Sep 18;11:574862. doi: 10.3389/fimmu.2020.574862. eCollection 2020.
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Arterioscler Thromb Vasc Biol. 2020 Oct;40(10):2404-2407. doi: 10.1161/ATVBAHA.120.314860. Epub 2020 Aug 7.
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The role of cytokine profile and lymphocyte subsets in the severity of coronavirus disease 2019 (COVID-19): A systematic review and meta-analysis.细胞因子谱和淋巴细胞亚群在 2019 年冠状病毒病(COVID-19)严重程度中的作用:系统评价和荟萃分析。
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新型冠状病毒肺炎患者肺部中性粒细胞募集和白细胞介素-8/白细胞介素-17A 组织表达。

Lung Neutrophilic Recruitment and IL-8/IL-17A Tissue Expression in COVID-19.

机构信息

Laboratory of Experimental Pathology, Postgraduate Program of Health Sciences, School of Medicine, Pontifícia Universidade Católica do Paraná, Curitiba, Brazil.

Postgraduate Program in Biotechnology Applied to Child and Adolescent Health, Faculdades Pequeno Príncipe, Instituto de Pesquisa Pelé Pequeno Príncipe, Curitiba, Brazil.

出版信息

Front Immunol. 2021 Mar 30;12:656350. doi: 10.3389/fimmu.2021.656350. eCollection 2021.

DOI:10.3389/fimmu.2021.656350
PMID:33868301
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8044579/
Abstract

The new SARS-CoV-2 virus differs from the pandemic Influenza A virus H1N1 subtype (H1N1pmd09) how it induces a pro-inflammatory response in infected patients. This study aims to evaluate the involvement of SNPs and tissue expression of IL-17A and the neutrophils recruitment in lung samples from patients who died of severe forms of COVID-19 comparing to those who died by H1N1pdm09. Twenty lung samples from patients SARS-CoV-2 infected (COVID-19 group) and 10 lung samples from adults who died from a severe respiratory H1N1pdm09 infection (H1N1 group) were tested. The tissue expression of IL-8/IL-17A was identified by immunohistochemistry, and hematoxylin and eosin (H&E) stain slides were used for neutrophil scoring. DNA was extracted from paraffin blocks, and genotyping was done in real time-PCR for two target polymorphisms. Tissue expression increasing of IL-8/IL-17A and a higher number of neutrophils were identified in samples from the H1N1 group compared to the COVID-19 group. The distribution of genotype frequencies in the gene was not statistically significant between groups. However, the G allele (GG and GA) of rs3819025 was correlated with higher tissue expression of IL-17A in the COVID-19 group. SARS-CoV-2 virus evokes an exacerbated response of the host's immune system but differs from that observed in the H1N1pdm09 infection since the IL-8/IL-17A tissue expression, and lung neutrophilic recruitment may be decreased. In SNP rs3819025 (G/A), the G allele may be considered a risk allele in the patients who died for COVID-19.

摘要

新型 SARS-CoV-2 病毒与大流行流感 A 型病毒 H1N1 亚型(H1N1pmd09)在感染患者中引发炎症反应的方式不同。本研究旨在评估 SNP 及 IL-17A 的组织表达和中性粒细胞在死于 COVID-19 重症患者肺组织中的募集情况,并与死于 H1N1pdm09 的患者进行比较。共检测了 20 例 SARS-CoV-2 感染患者(COVID-19 组)和 10 例死于严重 H1N1pdm09 感染的成人(H1N1 组)的肺组织样本。通过免疫组化鉴定 IL-8/IL-17A 的组织表达,并用苏木精和伊红(H&E)染色载玻片对中性粒细胞进行评分。从石蜡块中提取 DNA,并用实时 PCR 进行两个目标多态性的基因分型。与 COVID-19 组相比,H1N1 组的 IL-8/IL-17A 组织表达增加和中性粒细胞数量较多。两组之间基因的基因型频率分布无统计学差异。然而,rs3819025 基因的 G 等位基因(GG 和 GA)与 COVID-19 组中 IL-17A 的组织表达升高相关。SARS-CoV-2 病毒引发宿主免疫系统的过度反应,但与 H1N1pdm09 感染不同,因为 IL-8/IL-17A 的组织表达和肺中性粒细胞募集可能减少。在 SNP rs3819025(G/A)中,G 等位基因可能被认为是 COVID-19 死亡患者的风险等位基因。