The role of bacteria in airway inflammation in exacerbations of chronic obstructive pulmonary disease

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Abstract
Bacteria cause approximately half of all chronic obstructive pulmonary disease exacerbations. The purpose of this review is to evaluate the status of research on the role of bacteria in airway inflammation during exacerbations and the mechanisms by which bacterial antigens induce inflammation. Bacteria in the airways of adults with chronic obstructive pulmonary disease release antigens including endotoxin, peptidoglycan fragments, lipoproteins, and other molecules into the airways. These bacterial antigens induce potent inflammatory effects in the airways. Bacterial exacerbations are associated with systemic inflammation. Studies of Haemophilus influenzae, the most common bacterial cause of exacerbations, reveal that strains associated with exacerbations induce more inflammation compared to colonizing strains. H. influenzae antigens induce production of interleukin-8 and tumor necrosis factor-alpha, activate Toll-like 2 receptors, activate NFκB and p38 mitogen-activated protein signaling pathways, and have other inflammatory effects. Research on the role of bacteria in causing inflammation in chronic obstructive pulmonary disease has been neglected for decades. Research should be directed at further evaluating the role of bacterial antigens in airway inflammation. Reducing or modulating bacterial infection of the airways in chronic obstructive pulmonary disease has the potential to reduce airway inflammation by eliminating an important inciting cause.