Airway inflammation in nonobstructive and obstructive chronic bronchitis with chronic haemophilus influenzae airway infection. Comparison with noninfected patients with chronic obstructive pulmonary disease.
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.
Bresser
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Departments of Pulmonology and Clinical Microbiology, and Clinical and Laboratory Immunology Unit, Academic Medical Center, University of Amsterdam, The Netherlands.
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van Alphen
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Jansen
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Lutter
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D001991:Bronchitis / Q000175:diagnosis* / Q000503:physiopathology; D005260:Female; D006192:Haemophilus Infections / Q000175:diagnosis* / Q000503:physiopathology; D006193:Haemophilus influenzae; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D008173:Lung Diseases, Obstructive / Q000175:diagnosis* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012141:Respiratory Tract Infections / Q000175:diagnosis* / Q000503:physiopathology; D018746:Systemic Inflammatory Response Syndrome / Q000175:diagnosis* / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha