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


RESULTS
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 NFkappaB and p38 mitogen-activated protein signaling pathways, and have other inflammatory effects.


CONCLUSIONS
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.
Murphy
Timothy F
TF
Division of Infectious Diseases, University at Buffalo, State University of New York and Veterans Affairs Western New York Healthcare System, Buffalo, New York, USA. murphyt@buffalo.edu
D000328:Adult; D001424:Bacterial Infections / Q000276:immunology / Q000473:pathology*; D001992:Bronchoalveolar Lavage Fluid / Q000382:microbiology; D006193:Haemophilus influenzae / Q000254:growth & development / Q000276:immunology; D006801:Humans; D011014:Pneumonia / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D013183:Sputum / Q000382:microbiology