Change in inflammation in out-patient COPD patients from stable phase to a subsequent exacerbation.
BACKGROUND
Inflammation increases during exacerbations of COPD, but only a few studies systematically assessed these changes. Better identification of these changes will increase our knowledge and potentially guide therapy, for instance by helping with quicker distinction of bacterially induced exacerbations from other causes.


OBJECTIVE
To identify which inflammatory parameters increase during COPD exacerbations compared to stable disease, and to compare bacterial and non-bacterial exacerbations.


METHODS
In 45 COPD patients (37 male/8 female, 21 current smokers, mean age 65, FEV(1) 52% predicted, pack years 38) sputum was collected during a stable phase and subsequently during an exacerbation.


RESULTS
Sputum total cell counts (9.0 versus 7.9 x 10(6)/mL), eosinophils (0.3 versus 0.2 x 10(6)/mL), neutrophils (6.1 versus 5.8 x 10(6)/mL), and lymphocytes (0.07 versus 0.02 x 10(6)/mL) increased significantly during an exacerbation compared to stable disease. A bacterial infection was demonstrated by culture in 8 sputum samples obtained during an exacerbation. These exacerbations had significantly increased sputum total cell and neutrophil counts, leukotriene-B4, myeloperoxidase, interleukin-8 and interleukin-6, and tumor necrosis factor-alpha (TNF-alpha) levels, and were also associated with more systemic inflammation compared to exacerbations without a bacterial infection. Sputum TNF-alpha level during an exacerbation had the best test characteristics to predict a bacterial infection.


CONCLUSIONS
Sputum eosinophil, neutrophil, and lymphocyte counts increase during COPD exacerbations. The increase in systemic inflammation during exacerbations seems to be limited to exacerbations caused by bacterial infections of the lower airways. Sputum TNF-alpha is a candidate marker for predicting airway bacterial infection.
Department of Pulmonology, Groningen Research Institute for Asthma and COPD (GRIAC), University Medical Center Groningen, University of Groningen, the Netherlands.
Erik
E
Bathoorn
Jeroen J W
JJ
Liesker
Dirkje S
DS
Postma
Gerard H
GH
Koëter
Marco
M
van der Toorn
Sicco
S
van der Heide
H Alec
HA
Ross
Antoon J M
AJ
van Oosterhout
Huib A M
HA
Kerstjens
D000368:Aged; D016207:Cytokines / Q000097:blood / Q000378:metabolism*; D004804:Eosinophils / Q000276:immunology; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism*; D007958:Leukocyte Count; D007962:Leukocytes / Q000276:immunology* / Q000382:microbiology; D008168:Lung / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology; D008214:Lymphocytes / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology; D010045:Outpatients; D011014:Pneumonia / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology; D013183:Sputum / Q000276:immunology / Q000382:microbiology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016207:Cytokines; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha