Airway inflammation in nonobstructive and obstructive chronic bronchitis with chronic Haemophilus influenzae airway infection: Comparison with noninfected patients with chronic obstructive pulmonary disease

• Published in: American journal of respiratory and critical care medicine Vol. 162; no. 3; pp. 947 - 952
• Main Authors: BRESSER, Paul, OUT, Theo A, VAN ALPHEN, Loek, JANSEN, Henk M, LUTTER, René
• Format: Journal Article
• Language: English
• Published: New York, NY American Lung Association 01-09-2000
• Subjects: Biological and medical sciences; Bronchitis - diagnosis; Bronchitis - physiopathology; Chronic obstructive pulmonary disease, asthma; Female; Haemophilus Infections - diagnosis; Haemophilus Infections - physiopathology; Haemophilus influenzae; Humans; Inflammation Mediators - blood; Lung Diseases, Obstructive - diagnosis; Lung Diseases, Obstructive - physiopathology; Male; Medical sciences; Middle Aged; Pneumology; Respiratory Tract Infections - diagnosis; Respiratory Tract Infections - physiopathology; Systemic Inflammatory Response Syndrome - diagnosis; Systemic Inflammatory Response Syndrome - physiopathology; Tumor Necrosis Factor-alpha - metabolism; Human; Lung disease; Respiratory disease; Biological marker; Haemophilus influenzae; Pasteurellaceae; Infection; Chronic; Sputum; Bacteria; Bronchus disease; Bronchitis; Obstructive pulmonary disease; Comparative study; Tumor necrosis factor α
• ISSN: 1073-449X; 1535-4970
• DOI: 10.1164/ajrccm.162.3.9908103

Nonencapsulated Haemophilus influenzae often causes chronic infections of the lower respiratory tract in both nonobstructive and obstructive chronic bronchitis. We assessed airway inflammation in clinically stable, chronically H. influenzae-infected patients with nonobstructive (CB-HI, n = 10) and in patients with obstructive chronic bronchitis (COPD-HI, n = 10) by analyses of the sol phase of spontaneously expectorated sputum (SSP). As compared with the CB-HI group, the COPD-HI group had significantly higher (p < 0.05) levels of myeloperoxidase (MPO) and tumor necrosis factor (TNF)-alpha in their SSP, whereas the degree of plasma protein leakage (SSP-to-serum ratio of plasma proteins) and the levels of interleukin (IL)-8, secretory IgA, and lactoferrin were similar in the two groups. These findings point to differences in pathophysiology in CB-HI and COPD-HI. The high level of TNF-alpha in the SSP of COPD-HI patients is in accord with the proposed role of TNF-alpha in the development of airway obstruction in COPD patients. In apparent contradiction, low levels of TNF-alpha were found in the SSP of noninfected but otherwise similar COPD patients (n = 9). This finding, however, does not exclude an exaggerated TNF-alpha response to infection or another stimulus in the airways of COPD patients. The SSP levels of MPO and IL-8, and the degree of plasma protein leakage in the COPD-HI group, were retrospectively compared with and found significantly higher than those of noninfected COPD patients, suggesting a more marked inflammatory response in COPD-HI. Whether this reflects a direct cause-and-effect relationship should be addressed in a future long-term prospective study involving repeated measurements in the same patients.