tetano
Editor, Senior Moderator
Dis Markers
. 2021 Sep 28;2021:6803510.
doi: 10.1155/2021/6803510. eCollection 2021.
Effect of ORF7 of SARS-CoV-2 on the Chemotaxis of Monocytes and Neutrophils In Vitro
Gang Wang[SUP] 1 [/SUP], Jun Guan[SUP] 1 [/SUP], Guojun Li[SUP] 2 [/SUP], Fengtian Wu[SUP] 1 [/SUP], Qin Yang[SUP] 1 [/SUP], Chunhong Huang[SUP] 1 [/SUP], Junwei Shao[SUP] 1 [/SUP], Lichen Xu[SUP] 1 [/SUP], Zixuan Guo[SUP] 1 [/SUP], Qihui Zhou[SUP] 1 [/SUP], Haihong Zhu[SUP] 1 [/SUP], Zhi Chen[SUP] 1 [/SUP]
Affiliations
Abstract
Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently the most significant public health threat worldwide. Patients with severe COVID-19 usually have pneumonia concomitant with local inflammation and sometimes a cytokine storm. Specific components of the SARS-CoV-2 virus trigger lung inflammation, and recruitment of immune cells to the lungs exacerbates this process, although much remains unknown about the pathogenesis of COVID-19. Our study of lung type II pneumocyte cells (A549) demonstrated that ORF7, an open reading frame (ORF) in the genome of SARS-CoV-2, induced the production of CCL2, a chemokine that promotes the chemotaxis of monocytes, and decreased the expression of IL-8, a chemokine that recruits neutrophils. A549 cells also had an increased level of IL-6. The results of our chemotaxis Transwell assay suggested that ORF7 augmented monocyte infiltration and reduced the number of neutrophils. We conclude that the ORF7 of SARS-CoV-2 may have specific effects on the immunological changes in tissues after infection. These results suggest that the functions of other ORFs of SARS-CoV-2 should also be comprehensively examined.
. 2021 Sep 28;2021:6803510.
doi: 10.1155/2021/6803510. eCollection 2021.
Effect of ORF7 of SARS-CoV-2 on the Chemotaxis of Monocytes and Neutrophils In Vitro
Gang Wang[SUP] 1 [/SUP], Jun Guan[SUP] 1 [/SUP], Guojun Li[SUP] 2 [/SUP], Fengtian Wu[SUP] 1 [/SUP], Qin Yang[SUP] 1 [/SUP], Chunhong Huang[SUP] 1 [/SUP], Junwei Shao[SUP] 1 [/SUP], Lichen Xu[SUP] 1 [/SUP], Zixuan Guo[SUP] 1 [/SUP], Qihui Zhou[SUP] 1 [/SUP], Haihong Zhu[SUP] 1 [/SUP], Zhi Chen[SUP] 1 [/SUP]
Affiliations
- PMID: 34603560
- PMCID: PMC8483903
- DOI: 10.1155/2021/6803510
Abstract
Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently the most significant public health threat worldwide. Patients with severe COVID-19 usually have pneumonia concomitant with local inflammation and sometimes a cytokine storm. Specific components of the SARS-CoV-2 virus trigger lung inflammation, and recruitment of immune cells to the lungs exacerbates this process, although much remains unknown about the pathogenesis of COVID-19. Our study of lung type II pneumocyte cells (A549) demonstrated that ORF7, an open reading frame (ORF) in the genome of SARS-CoV-2, induced the production of CCL2, a chemokine that promotes the chemotaxis of monocytes, and decreased the expression of IL-8, a chemokine that recruits neutrophils. A549 cells also had an increased level of IL-6. The results of our chemotaxis Transwell assay suggested that ORF7 augmented monocyte infiltration and reduced the number of neutrophils. We conclude that the ORF7 of SARS-CoV-2 may have specific effects on the immunological changes in tissues after infection. These results suggest that the functions of other ORFs of SARS-CoV-2 should also be comprehensively examined.