Enhanced PMN response in chronic bronchitis and community-acquired pneumonia.
Chronic bronchitis is a frequent underlying disease in community-acquired pneumonia (CAP). It is unclear to what extent an impaired or exaggerated innate immune response contributes to disease manifestations and severity. To assess the role of neutrophil activation and recruitment during acute pneumonic episodes, peripheral polymorphonulcear neutrophil (PMN) activation, chemotactic activity, interleukin-8 (CXCL-8) and CXCL-8 receptor (CXCR) expression and apoptosis rate were evaluated in CAP patients with and without chronic bronchitis. In addition, the expression of CXCRs and CXCL-8 was assessed on pulmonary neutrophils in chronic bronchitis patients to compare the activation of the chemokine system in different compartments. CAP severity was assessed by the simplified acute physiology score II and the prognosis of disease was assessed by the pneumonia severity index (PSI). An increased chemotactic activity of PMN from chronic bronchitis patients with CAP was found, which was not related to the expression of CXCRs. In addition, a decreased apoptosis rate of PMN was observed. Chemotactic activity was related to the PSI. Comparison of peripheral and pulmonary PMN revealed enhanced CXCL-8 levels and a decreased CXCR expression in the lung. In conclusion, neutrophil function in patients with chronic bronchitis and community-acquired pneumonia is characterised by an increased chemotactic activity combined with a decreased apoptosis rate. The downregulation of interleukin-8 receptors in the pulmonary compartment deserves further investigation.
Strassburg
A
A
III. Dept of Medicine, University of Luebeck, Ratzeburger Allee 160, 23538 Luebeck, Germany. alan.strassburg@gmx.de
Droemann
D
D
van Zandbergen
G
G
Kothe
H
H
Dalhoff
K
K
D000368:Aged; D017209:Apoptosis; D001991:Bronchitis / Q000150:complications / Q000276:immunology*; D002634:Chemotaxis, Leukocyte / Q000276:immunology; D002908:Chronic Disease; D017714:Community-Acquired Infections / Q000209:etiology / Q000276:immunology*; D005260:Female; D006801:Humans; D016209:Interleukin-8 / Q000032:analysis; D008297:Male; D009504:Neutrophils / Q000276:immunology*; D011014:Pneumonia / Q000209:etiology / Q000276:immunology*; D023063:Receptors, Interleukin-8B
D016209:Interleukin-8; D023063:Receptors, Interleukin-8B