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Human rhinovirus (HRV) may cause severe exacerbations of asthma, which is accompanied by increased airway IL-33 concentrations. The aim of the study was to analyze the effect of IL-33 on the HRV-induced inflammatory response by the lung vascular endothelium. Human pulmonary microvascular endothelial cells (HMVEC-L) were exposed to HRV-16 alone or in the presence of IL-33. Number of HRV-16 copies in HMVEC-L, cytokines, chemokines and growth factors mRNA expression were assessed in real-time PCR. Protein concentrations were assessed in BioPlex. HRV16 strongly increased the release of plenty of inflammatory cytokines, including IL-1β, IL-6, TNF-α, RANTES and IP-10, chemokines: MIP-1α, MIP-1β, IL-8 and eotaxin as well as growth factors: G-CSF, GM-CSF, FGF and VEGF. Furthermore, HRV16 enhanced both mRNA expression and protein release of type I interferons. It also increased production: IL-12, IFN-γ, IL-4, IL-5, IL-13, IL-17, but not IL-10. IL-33 increased the capture of HRV16 particles associated with the increase of ICAM-1 expression. IL-33 increased the HRV16-induced release of IL-1β, IL-6; it did not affect RANTES, IP-10, TNF-α production. IL-33 enhanced HRV16-induced release of growth factors and chemokines – not affecting MIP-1β and MCP-1. Finally, IL-33 enhanced HRV16-induced release IL-12 (not IFN-γ), IL-4, IL-5, IL-13, IL-17, and IL-10. (p<0.05) IL-33 may augment the effect of rhinovirus HRV16 on inflammatory, but not antiviral, activity of the lung vascular endothelium, and thus lead to the heavy exacerbations of asthma. National Science Center 2017/25/B/NZ5/01575