Infections with pso variants (especially with the HK2 variant lacking O-Ag biosynthesis) activated endothelial cells with abundant expression of cell adhesion molecules (ICAM-1 and VCAM-1) and inflammatory mediators (CCL2, CXCL1, CXCL8, CCL20, and IL-6). The gene discussed is CXCL1; the disease is infection.