Airway Inflammation and Etiology of Acute Exacerbations of Chronic Bronchitis

Study objectives: The etiologic role of bacterialpathogens isolated from sputum culture in 40 to 50% of acuteexacerbations of chronic bronchitis (AECB) is controversial. Ifbacterial pathogens cause these AECB, they should be associated withgreater neutrophilic airway inflammation than pathogen-negativeexacerbations. Design: This hypothesis was tested bycomparing levels of interleukin (IL)-8, tumor necrosis factor(TNF)-α, and neutrophil elastase (NE) in 81 sputum samples obtainedfrom 45 patients with AECB. Four groups were compared. In the firstthree groups, nontypeable Haemophilus influenzae(n = 20), Haemophilus parainfluenzae (n = 27), andMoraxella catarrhalis (n = 14) were isolated as solepathogens, respectively. In the fourth group, only normal flora wasisolated (n = 20). Paired samples, obtained from individual patientsat different times, that differed in their culture results were alsocompared. Setting: An outpatient research clinic at a, Veterans Affairs Medical Center. Patients: Thesepatients were participating in a prospective, longitudinal study of thedynamics of bacterial infection in chronic bronchitis, for which theywere seen in the study clinic on a monthly basis as well as when theywere experiencing symptoms suggestive of AECB. Interventions: None. Measurements andresults: H influenzae exacerbations wereassociated with significantly higher sputum IL-8, TNF-α, and NE.M catarrhalis exacerbations demonstrated significantlyhigher sputum TNF-α and NE when compared to pathogen-negativeexacerbations. H parainfluenzae-associated exacerbationshad an inflammatory profile similar to pathogen-negative exacerbations. Sputum elastase level distinguished bacterial from nonbacterial AECBand correlated with clinical severity of the AECB. Conclusions: Increased airway inflammation associated withisolation of H influenzae and Mcatarrhalis supports an etiologic role of these pathogens in, AECB. The etiologic role of bacterialpathogens isolated from sputum culture in 40 to 50% of acuteexacerbations of chronic bronchitis (AECB) is controversial. Ifbacterial pathogens cause these AECB, they should be associated withgreater neutrophilic airway inflammation than pathogen-negativeexacerbations. This hypothesis was tested bycomparing levels of interleukin (IL)-8, tumor necrosis factor(TNF)-α, and neutrophil elastase (NE) in 81 sputum samples obtainedfrom 45 patients with AECB. Four groups were compared. In the firstthree groups, nontypeable Haemophilus influenzae(n = 20), Haemophilus parainfluenzae (n = 27), andMoraxella catarrhalis (n = 14) were isolated as solepathogens, respectively. In the fourth group, only normal flora wasisolated (n = 20). Paired samples, obtained from individual patientsat different times, that differed in their culture results were alsocompared. An outpatient research clinic at a, Veterans Affairs Medical Center. Thesepatients were participating in a prospective, longitudinal study of thedynamics of bacterial infection in chronic bronchitis, for which theywere seen in the study clinic on a monthly basis as well as when theywere experiencing symptoms suggestive of AECB. None. H influenzae exacerbations wereassociated with significantly higher sputum IL-8, TNF-α, and NE.M catarrhalis exacerbations demonstrated significantlyhigher sputum TNF-α and NE when compared to pathogen-negativeexacerbations. H parainfluenzae-associated exacerbationshad an inflammatory profile similar to pathogen-negative exacerbations. Sputum elastase level distinguished bacterial from nonbacterial AECBand correlated with clinical severity of the AECB. Increased airway inflammation associated withisolation of H influenzae and Mcatarrhalis supports an etiologic role of these pathogens in, AECB.