Several pro-inflammatory mediators including lipopolysaccharides (LPS) could trigger acute lung inflammation during bacterial infections, through upregulation of adhesion molecules (e.g., intercellular cell adhesion protein 1 (ICAM-1) and vascular cell adhesion protein-1 (VCAM-1)) [1,2,7,8], leading to the recruitment of polymorphonuclear (PMN) cells to inflammatory tissues and airway fluid [9,10]. This evidence concerns the gene VCAM1 and bacterial infectious disease.