To unravel the effect of VIP in the setting of SARS-CoV-2, we hypothesized that VIP might influence the inflammatory response of different epithelial cells (e.g., CaCo-2, A549 and BEAS-2B) upon viral infection, which was in vitro assessed by stimulating cells with either a TLR3 (Toll-like receptor 3) agonist (Poly I:C), SARS-CoV-2 spike protein or a combination of both. Here, VIP is linked to viral infectious disease.