title: Airway inflammation and etiology of acute exacerbations of chronic bronchitis.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  This hypothesis was tested by comparing levels of interleukin (IL)-8, tumor necrosis factor (TNF)-alpha, and neutrophil elastase (NE) in 81 sputum samples obtained from 45 patients with AECB. Four groups were compared. In the first three groups, nontypable 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.
  
  
  METHODS
  An outpatient research clinic at a Veterans Affairs Medical Center.
  
  
  METHODS
  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.
  
  
  METHODS
  None.
  
  
  RESULTS
  H influenzae exacerbations were associated with significantly higher sputum IL-8, TNF-alpha, and NE. M catarrhalis exacerbations demonstrated significantly higher sputum TNF-alpha 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.
authors: Department of Veterans Affairs Western New York Healthcare System, Buffalo, NY 14215, USA.
authors: S
authors: S
authors: Sethi
authors: K
authors: K
authors: Muscarella
authors: N
authors: N
authors: Evans
authors: K L
authors: KL
authors: Klingman
authors: B J
authors: BJ
authors: Grant
authors: T F
authors: TF
authors: Murphy
mesh_terms: D000208:Acute Disease; D000368:Aged; D000369:Aged, 80 and over; D001991:Bronchitis / Q000382:microbiology / Q000473:pathology* / Q000503:physiopathology; D002908:Chronic Disease; D005340:Fibrinogen / Q000032:analysis; D006190:Haemophilus / Q000302:isolation & purification; D006193:Haemophilus influenzae / Q000302:isolation & purification; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D019272:Leukocyte Elastase / Q000032:analysis; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D001936:Moraxella catarrhalis / Q000302:isolation & purification; D011446:Prospective Studies; D013183:Sputum / Q000737:chemistry / Q000166:cytology / Q000382:microbiology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D018836:Inflammation Mediators; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D005340:Fibrinogen; D019272:Leukocyte Elastase