Key result
Human rhinovirus 16 infection of human vascular endothelial cells increased antiviral and inflammatory responses, including IFN-β, RANTES, and IP-10 expression.
Why the study?
The effect of rhinovirus on airway epithelium is well described, but its influence on the vascular endothelium is unknown.
The vascular endothelium can be infected by human rhinovirus and generate an antiviral and inflammatory innate response, indicating possible involvement in airway infection immunopathology.
Endothelium may contribute to rhinovirus immunopathology; leaves open its role in human airway disease.
The effect of rhinovirus on airway epithelium is very well described. However, its influence on the vascular endothelium is unknown. The current study assesses the effect of rhinovirus HRV16 on the antiviral and inflammatory response in the human vascular endothelial cells (ECs). HRV16 increased IFN-β, RANTES, and IP-10 mRNA expression and protein release. HRV16 copy number in ECs reached maximal value 10 h after incubation. Increase in virus copies was accompanied by the enhancement of Toll- and RIG-I-like receptors: TLR3, RIG-I, and MDA5. Additionally, HRV16 increased OAS-1 and PKR mRNA expression, enzymes responsible for virus degradation and inhibition of replication. ICAM-1 blockade decreased HRV16 copy number in ECs and inhibited IFN-β, RANTES, IP-10, OAS1, PKR, TLR3, RIG-I, and MDA5 mRNA expression increase upon subsequent induction with HRV16. The vascular endothelium may be infected by human rhinovirus and generate antiviral and inflammatory innate response. Results of the study indicate the possible involvement of the vascular endothelium in the immunopathology of rhinoviral airway infections.
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Chałubiński et al. (2020) studied Rhinovirus infection. Human rhinovirus 16 (HRV16) was evaluated on Antiviral and inflammatory response (IFN-β, RANTES, IP-10 mRNA expression and protein release). Human rhinovirus 16 infection of human vascular endothelial cells increased antiviral and inflammatory responses, including IFN-β, RANTES, and IP-10 expression.
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