变异株 SARS-CoV-2 突变刺突蛋白的多种促炎能力。
Diverse pro-inflammatory ability of mutated spike protein derived from variant strains of SARS-CoV-2.
机构信息
Department of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan.
出版信息
Cytokine. 2024 Jun;178:156592. doi: 10.1016/j.cyto.2024.156592. Epub 2024 Apr 3.
The severity of COVID-19 has been reported to differ among SARS-CoV-2 mutant variants. The overactivation of macrophages is involved in severe COVID-19, yet the effects of SARS-CoV-2 mutations on macrophages remain poorly understood. To clarify the effects, we examined whether mutations of spike proteins (S-proteins) affect macrophage activation. CD14 monocyte-derived macrophages were stimulated with the recombinant S-protein of the wild-type, Delta, and Omicron strains or live viral particles of individual strains. Regarding IL-6 and TNF-α, Delta or Omicron S-protein had stronger or weaker pro‑inflammatory ability, respectively, than the wild-type. Similar trends were observed between S-proteins and viral particles. S-protein mutations could be related to the diversity in macrophage activation and severity rates in COVID-19 caused by various SARS-CoV-2 strains.
据报道，SARS-CoV-2 突变株之间的 COVID-19 严重程度不同。巨噬细胞的过度激活与严重的 COVID-19 有关，但 SARS-CoV-2 突变对巨噬细胞的影响仍知之甚少。为了阐明其影响，我们研究了刺突蛋白（S 蛋白）突变是否影响巨噬细胞的激活。用野生型、Delta 和奥密克戎株的重组 S 蛋白或单个毒株的活病毒颗粒刺激 CD14 单核细胞衍生的巨噬细胞。关于白细胞介素 6 和肿瘤坏死因子-α，Delta 或奥密克戎 S 蛋白的促炎能力分别强于或弱于野生型。在 S 蛋白和病毒颗粒之间也观察到了类似的趋势。S 蛋白突变可能与不同 SARS-CoV-2 株引起的 COVID-19 中巨噬细胞激活和严重程度的多样性有关。
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