The TNF-α–ICAM-1–MCP-1 axis may represent a conserved pathway for inflammatory amplification in the lung; however, further in vivo and patient-based studies will be required to determine whether these mechanisms operate across disease contexts such as pneumonia, asthma, acute lung injury, and pollutant exposure where TLR2 and TLR4 ligands play important roles (47–49). This evidence concerns the gene CCL2 and susceptibility to pneumonia measurement.