During the development of asthma, which involves an aberrant airway immune response, insults such as infection, allergens, or environmental factors could alter the profile of BECs, initiating chronic inflammation by polarizing T-helper type 2 (Th2) lymphocytes and promoting the secretion of proinflammatory proteins, including eotaxin-1, monocyte chemoattractant protein-1 (MCP-1), interleukin- (IL-) 8, and intercellular adhesion molecule-1 (ICAM-1) [7–9]. This evidence concerns the gene ICAM1 and infection.