Cardiomyocytes recruit monocytes upon SARS-CoV-2 infection by secreting CCL2.

Cardiomyocytes recruit monocytes upon SARS-CoV-2 infection by secreting CCL2.
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DOI:
10.1016/j.stemcr.2021.07.012
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发表时间:
2021-09-14
期刊:
影响因子:
5.9
通讯作者:
Chen S
Chen S
中科院分区:
医学1区
文献类型:
--
作者:
Yang L;Nilsson-Payant BE;Han Y;Jaffré F;Zhu J;Wang P;Zhang T;Redmond D;Houghton S;Møller R;Hoagland D;Carrau L;Horiuchi S;Goff M;Lim JK;Bram Y;Richardson C;Chandar V;Borczuk A;Huang Y;Xiang J;Ho DD;Schwartz RE;tenOever BR;Evans T;Chen S

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Heart injury has been reported in up to 20% of COVID-19 patients, yet the cause of myocardial histopathology remains unknown. Here, using an established in vivo hamster model, we demonstrate that SARS-CoV-2 can be detected in cardiomyocytes of infected animals. Furthermore, we found damaged cardiomyocytes in hamsters and COVID-19 autopsy samples. To explore the mechanism, we show that both human pluripotent stem cell-derived cardiomyocytes (hPSC-derived CMs) and adult cardiomyocytes (CMs) can be productively infected by SARS-CoV-2, leading to secretion of the monocyte chemoattractant cytokine CCL2 and subsequent monocyte recruitment. Increased CCL2 expression and monocyte infiltration was also observed in the hearts of infected hamsters. Although infected CMs suffer damage, we find that the presence of macrophages significantly reduces SARS-CoV-2-infected CMs. Overall, our study provides direct evidence that SARS-CoV-2 infects CMs in vivo and suggests a mechanism of immune cell infiltration and histopathology in heart tissues of COVID-19 patients. SARS-CoV-2 is detected in cardiomyocytes of SARS-CoV-2-infected hamsters SARS-CoV-2-infected human cardiomyocytes secrete CCL2 SARS-CoV-2-infected cardiomyocytes recruit monocytes by secreting CCL2 Macrophages decrease SARS-CoV-2 infection by engulfing infected CMs In this article, Dr. Shuibing Chen and colleagues report the direct evidence of SARS-CoV-2 infection of cardiomyocytes in vivo and establish an in vitro model to study immune cell infiltration. They suggest that SARS-CoV-2 infection leads to secretion of CCL2, which recruits monocyte migration.
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