The hyperactivation of the immune system could result in acute respiratory distress syndrome. We used serum from clinically well-characterized COVID-19 patients with severe (n=10) and moderate (n=9) disease to analyze which profiles and levels of pro- and anti-inflammatory markers affect human microvascular lung endothelial (EC) and bronchial epithelial (EpC) cells, in vitro. According to the cytokine/chemokine/inflammatory marker multiplex assay, most of the markers were elevated in severe patients whereas statistically higher levels were found only for soluble ICAM-1 and IL-17. Next, serum from each patient was added to EC (5%) and EpC (2%) for 18 h. We observed a marked induction of IL-8/CXCL8 release and expression in EpC and EC exposed to the serum of severe but not moderate COVID-19 patients. We also analyzed cell responses to patient serum based on the levels of inflammatory markers, independently of the disease severity. Serum containing higher levels of chemokines (IL-8 and MCP-1), and soluble ICAM-1 significantly activated both lung EC and EpC. Specifically, serum containing higher levels of soluble ICAM-1 increased FITM2 mRNA in EpC and VEGFA mRNA in EC. The EC treated with serum containing less MCP-1 and IL-8 showed a higher expression of PECAM1. We demonstrate divergent responses of EC and EpC to patient serum containing different levels and profiles of inflammation markers and that in vitro models of human lung cells can be useful to study respiratory system injuries.