期刊
JOURNAL OF INFECTIOUS DISEASES
卷 224, 期 8, 页码 1333-1344出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiab400
关键词
adult; children; COVID-19; lymphopenia; mitochondria apoptosis
资金
- National Natural Science Foundation of China [31470877]
- National Science and Technology Key Projects for Major Infectious Diseases [2017ZX10302301-002]
- Support Scheme of Guangzhou for Leading Talents in Innovation and Entrepreneurship [2017004]
- Guangdong Scientific and Technological Research Project for Prevention and Treatment of COVID-19 [2020A111128022, 2020B111112003]
- Guangdong Scientific and Technological Research Special Fund for COVID-19 [202020012612200001]
- Zhuhai Scientific and Technological Research Project for COVID-19 Containment [ZH22036302200029PWC]
- Zhuhai Industrial Technological Research and Development Project for Prevention and Treatment of COVID-19 [ZH22046301200018PWC]
- Science and Technology Planning Project of Guangzhou [201704020226, 201604020006]
- Development Project of Foshan Fourth People's Hospital [FSSYKF-2020003, FSSYKF-2020017]
The apoptosis of peripheral T cells in COVID-19 adult patients was identified to cause mitochondrial apoptosis, induced by elevated tumor necrosis factor-alpha and interleukin-6 levels in COVID-19 plasma, leading to DNA damage. In contrast, child T cells showed tolerance to mitochondrial apoptosis due to mitochondria autophagy, indicating a difference in response mechanisms between adults and children infected with SARS-CoV-2.
Background. Lymphopenia is a key feature for adult patients with coronavirus disease 2019 (COVID-19), although it is rarely observed in children. The underlying mechanism remains unclear. Methods. Immunohistochemical and flow cytometric analyses were used to compare the apoptotic rate of T cells from COVID-19 adults and children and apoptotic responses of adult and child T cells to COVID-19 pooled plasma. Biological properties of caspases and reactive oxygen species were assessed in T cells treated by COVID-19 pooled plasma. Results. Mitochondria apoptosis of peripheral T cells were identified in COVID-19 adult patient samples but not in the children. Furthermore, increased tumor necrosis factor-alpha and interleukin-6 in COVID-19 plasma induced mitochondria apoptosis and caused deoxyribonucleic acid damage by elevating reactive oxygen species levels of the adult T cells. However, the child T cells showed tolerance to mitochondrial apoptosis due to mitochondria autophagy. Activation of autophagy could decrease apoptotic sensitivity of the adult T cells to plasma from COVID-19 patients. Conclusions. Our results indicated that the mitochondrial apoptosis pathway was activated in T cells of COVID-19 adult patients specifically, which may shed light on the pathophysiological difference between adults and children infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
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