Decreased apoptosis and increased activation of alveolar neutrophils in bacterial pneumonia.
OBJECTIVE
The central role of apoptosis in the regulation of lung inflammation is increasingly recognized. The aim of this study was to determine the parameters of cell activation and apoptosis on neutrophils from the circulation and the pulmonary compartment in patients with community-acquired pneumonia (CAP), and to assess the role of the Fas system and of complement-regulating molecules in this context.


METHODS
The study population consisted of nine patients with CAP (group 1) and six age-matched control patients without evidence of bronchopulmonary inflammation (group 2). Apoptosis rate and expression of CD11b, CD16, CD55, CD59, CD95, and CD114 surface molecules on systemic and bronchoalveolar neutrophils were assessed ex vivo using fluorescence-activated cell sorter analysis.


RESULTS
In patients with CAP, we found a significant decrease of the mean apoptosis rate in pulmonary neutrophils compared to systemic neutrophils, without concomitant changes in Fas expression. In contrast, cell activation markers were significantly increased on pulmonary cells (CD11b, 288 +/- 98.2 relative mean fluorescence intensity [rMFI] vs 53.8 +/- 10.8 rMFI on peripheral cells), and similar changes were observed with respect to the expression of complement-regulating molecules. Pulmonary polymorphonuclear neutrophils of the control group showed analogous changes, compared to systemic neutrophils, but a significantly higher rate of apoptosis and a lower increase of activation-marker expression were found, compared to pulmonary neutrophils of patients with pneumonia.


CONCLUSIONS
Pulmonary neutrophils from patients with CAP show a decreased rate of apoptosis and increased activation status in the alveolar compartment, which may be important for effective control of pulmonary inflammation.
Droemann
D
D
II. Department of Medicine, Medical University Luebeck, Germany.
Aries
S P
SP
Hansen
F
F
Moellers
M
M
Braun
J
J
Katus
H A
HA
Dalhoff
K
K
D048868:Adaptor Proteins, Signal Transducing; D000368:Aged; D017209:Apoptosis / Q000276:immunology*; D051017:Apoptosis Regulatory Proteins; D001999:Bronchoscopy; D002352:Carrier Proteins / Q000502:physiology; D017714:Community-Acquired Infections / Q000276:immunology*; D003167:Complement Activation / Q000276:immunology; D005260:Female; D006192:Haemophilus Infections / Q000276:immunology; D006801:Humans; D008297:Male; D008875:Middle Aged; D018375:Neutrophil Activation / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology; D018410:Pneumonia, Bacterial / Q000276:immunology*; D011018:Pneumonia, Pneumococcal / Q000276:immunology; D011650:Pulmonary Alveoli / Q000276:immunology*
D048868:Adaptor Proteins, Signal Transducing; D051017:Apoptosis Regulatory Proteins; D002352:Carrier Proteins; C490780:FAF1 protein, human