tetano
Editor, Senior Moderator
Front Public Health
. 2022 Feb 11;10:833967.
doi: 10.3389/fpubh.2022.833967. eCollection 2022.
Targeting TNF-α for COVID-19: Recent Advanced and Controversies
Yi Guo[SUP] 1 2 [/SUP], Ke Hu[SUP] 1 [/SUP], Yuxuan Li[SUP] 1 [/SUP], Chanjun Lu[SUP] 1 [/SUP], Ken Ling[SUP] 3 [/SUP], Chuanqi Cai[SUP] 1 [/SUP], Weici Wang[SUP] 1 [/SUP], Dawei Ye[SUP] 4 5 [/SUP]
Affiliations
Abstract
Recent advances in the pathophysiologic understanding of coronavirus disease 2019 (COVID-19) suggests that cytokine release syndrome (CRS) has an association with the severity of disease, which is characterized by increased tumor necrosis factor α (TNF-α), interleukin (IL)-6, IL-2, IL-7, and IL-10. Hence, managing CRS has been recommended for rescuing severe COVID-19 patients. TNF-α, one of the pro-inflammatory cytokines commonly upregulated in acute lung injury, triggers CRS and facilitates SARS-CoV-2 interaction with angiotensin-converting enzyme 2 (ACE2). TNF-α inhibitors, therefore, may serve as an effective therapeutic strategy for attenuating disease progression in severe SARS-CoV-2 infection. Below, we review the possibilities and challenges of targeting the TNF-α pathway in COVID-19 treatment.
Keywords: COVID-19; MIS-C; TNF-α inhibitor; cytokine release syndrome; infliximab.
. 2022 Feb 11;10:833967.
doi: 10.3389/fpubh.2022.833967. eCollection 2022.
Targeting TNF-α for COVID-19: Recent Advanced and Controversies
Yi Guo[SUP] 1 2 [/SUP], Ke Hu[SUP] 1 [/SUP], Yuxuan Li[SUP] 1 [/SUP], Chanjun Lu[SUP] 1 [/SUP], Ken Ling[SUP] 3 [/SUP], Chuanqi Cai[SUP] 1 [/SUP], Weici Wang[SUP] 1 [/SUP], Dawei Ye[SUP] 4 5 [/SUP]
Affiliations
- PMID: 35223745
- PMCID: PMC8873570
- DOI: 10.3389/fpubh.2022.833967
Abstract
Recent advances in the pathophysiologic understanding of coronavirus disease 2019 (COVID-19) suggests that cytokine release syndrome (CRS) has an association with the severity of disease, which is characterized by increased tumor necrosis factor α (TNF-α), interleukin (IL)-6, IL-2, IL-7, and IL-10. Hence, managing CRS has been recommended for rescuing severe COVID-19 patients. TNF-α, one of the pro-inflammatory cytokines commonly upregulated in acute lung injury, triggers CRS and facilitates SARS-CoV-2 interaction with angiotensin-converting enzyme 2 (ACE2). TNF-α inhibitors, therefore, may serve as an effective therapeutic strategy for attenuating disease progression in severe SARS-CoV-2 infection. Below, we review the possibilities and challenges of targeting the TNF-α pathway in COVID-19 treatment.
Keywords: COVID-19; MIS-C; TNF-α inhibitor; cytokine release syndrome; infliximab.