We observed no differences between healthy age matched controls and individuals with COPD in CXCL8 production in response to TLR agonists or E. coli. These results contrast with those of Culpitt et al [37] who found higher CXCL8 production in AM from COPD individuals in response to cigarette smoke extract and LPS, and Taylor et al [18] who showed that MDMs from people with COPD exhibited reduced phagocytosis of pathogens. The gene discussed is CXCL8; the disease is chronic obstructive pulmonary disease.