Surface expression of other adhesion molecules involved in neutrophil recruitment including CD54 (ICAM-1), CD102 (ICAM-2), CD106 (VCAM-1), and E-selectin is not upregulated on pulmonary endothelium following exposure to two different serotypes of Spn (Bullard et al., 1995; Moreland et al., 2004), suggesting these are not major drivers regulator of neutrophil influx during Spn infection. This evidence concerns the gene ICAM1 and infection.