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Clinical Investigations: COPD |

Airway Inflammation and Etiology of Acute Exacerbations of Chronic Bronchitis*

Sanjay Sethi, MD; Karen Muscarella, BS; Nancy Evans, RN; Karin L. Klingman, MD; Brydon J. B. Grant, MD, FCCP; Timothy F. Murphy, MD
Author and Funding Information

*From the Department of Veterans Affairs Western New York Healthcare System, Division of Pulmonary and Critical Care Medicine and Division of Infectious Diseases of the Department of Medicine, State University of New York at Buffalo, Buffalo, NY.

Correspondence to: Sanjay Sethi, MD, Department of Veterans Affairs Western New York Healthcare System (151), 3495 Bailey Ave, Buffalo, NY 14215



Chest. 2000;118(6):1557-1565. doi:10.1378/chest.118.6.1557
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Study objectives: The etiologic role of bacterial pathogens isolated from sputum culture in 40 to 50% of acute exacerbations of chronic bronchitis (AECB) is controversial. If bacterial pathogens cause these AECB, they should be associated with greater neutrophilic airway inflammation than pathogen-negative exacerbations.

Design: This hypothesis was tested by comparing levels of interleukin (IL)-8, tumor necrosis factor (TNF)-α, and neutrophil elastase (NE) in 81 sputum samples obtained from 45 patients with AECB. Four groups were compared. In the first three groups, nontypeable Haemophilus influenzae (n = 20), Haemophilus parainfluenzae (n = 27), and Moraxella catarrhalis (n = 14) were isolated as sole pathogens, respectively. In the fourth group, only normal flora was isolated (n = 20). Paired samples, obtained from individual patients at different times, that differed in their culture results were also compared.

Setting: An outpatient research clinic at a Veterans Affairs Medical Center.

Patients: These patients were participating in a prospective, longitudinal study of the dynamics of bacterial infection in chronic bronchitis, for which they were seen in the study clinic on a monthly basis as well as when they were experiencing symptoms suggestive of AECB.

Interventions: None.

Measurements and results:H influenzae exacerbations were associated with significantly higher sputum IL-8, TNF-α, and NE. M catarrhalis exacerbations demonstrated significantly higher sputum TNF-α and NE when compared to pathogen-negative exacerbations. H parainfluenzae-associated exacerbations had an inflammatory profile similar to pathogen-negative exacerbations. Sputum elastase level distinguished bacterial from nonbacterial AECB and correlated with clinical severity of the AECB.

Conclusions: Increased airway inflammation associated with isolation of H influenzae and M catarrhalis supports an etiologic role of these pathogens in AECB.

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