Key result
Treatment with IFN-γ significantly increased ACE-2 mRNA expression in primary cultures of normal human thyroid cells compared to untreated cells (p<0.001).
Why the study?
ACE-2 was demonstrated as the SARS-CoV-2 entry receptor and identified in thyroid cells, but the effect of pro-inflammatory cytokines on thyroid ACE-2 mRNA levels was unclear.
Does treatment with pro-inflammatory cytokines increase ACE-2 mRNA levels in human thyroid cells in primary cultures?
Does treatment with pro-inflammatory cytokines increase ACE-2 mRNA levels in human thyroid cells in primary cultures?
Pro-inflammatory cytokines IFN-γ and TNF-α increase ACE-2 mRNA levels in human thyroid cells, suggesting a potential mechanism for increased SARS-CoV-2 cellular entry during inflammation.
Answers are grounded in this paper and cite their sources.
May suggest inflammation enhances thyroid ACE-2 expression; leaves open clinical relevance for SARS-CoV-2 susceptibility.
INTRODUCTION: Angiotensin-converting-enzyme-2 (ACE-2) was demonstrated to be the receptor for cellular entry of SARS-CoV-2. ACE-2 mRNA was identified in several human tissues and recently also in thyroid cells in vitro. PURPOSE: Aim of the present study was to investigate the effect of pro-inflammatory cytokines on the ACE-2 mRNA levels in human thyroid cells in primary cultures. METHODS: Primary thyroid cell cultures were treated with IFN-γ and TNF-α alone or in combination for 24 h. ACE-2 mRNA levels were measured by RT-PCR. As a control, the levels of IFN-γ inducible chemokine (CXCL10) were measured in the respective cell culture supernatants. RESULTS: The mean levels of ACE-2 mRNA increased after treatment with IFN-γ and TNF-α in all the thyroid cell preparations, while the combination treatment did not consistently synergically increase ACE-2-mRNA. At difference, CXCL10 was consistently increased by IFN-γ and synergically further increased by the combination treatment with IFN-γ + TNF-α, with respect to IFN-γ alone. CONCLUSIONS: The results of the present study show that IFN-γ and, to a lesser extent TNF-α consistently increase ACE-2 mRNA levels in NHT primary cultures. More interestingly, the combined stimulation (proven to be effective according to the synergic effect registered for CXCL10) produces different responses in terms of ACE-2 mRNA modulation. These results would suggest that elevated levels of pro-inflammatory cytokines could facilitate the entering of the virus in cells by further increasing ACE-2 expression and/or account for the different degree of severity of SARS-COV-2 infection. This hypothesis deserves to be confirmed by further specific studies.
No takes yet. Share an insight, caveat, or question.
Coperchini et al. (2021) studied Normal human thyroid cells (in vitro) (n=6). IFN-γ and TNF-α vs. Not-treated (NT) cells was evaluated on ACE-2 mRNA levels (p=<0.001). Treatment with IFN-γ significantly increased ACE-2 mRNA expression in primary cultures of normal human thyroid cells compared to untreated cells (p<0.001).
Synapse has enriched 10 related papers. Consider them for comparative context: