Study objectives: The central role of apoptosis in the regulation of lung i
nflammation is increasingly recognized. The aim of this study was to determ
ine the parameters of cell activation and apoptosis on neutrophils from the
circulation and the pulmonary compartment in patients with community-acqui
red pneumonia (CAP), and to assess the role of the Fas system and of comple
ment-regulating molecules in this context.
Design and methods: The study population consisted of nine patients with CA
P (group 1) and six age-matched control patients without evidence of bronch
opulmonary inflammation (group 2). Apoptosis rate and expression of CD11b,
CD16, CD55, CD59, CD95, and CD114 surface molecules on systemic and broncho
alveolar neutrophils were assessed ex vivo using fluorescence-activated cel
l sorter analysis.
Results: In patients with CAP, we found a significant decrease of the mean
apoptosis rate in pulmonary neutrophils compared to systemic neutrophils, w
ithout 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 peri
pheral cells), and similar changes were observed with respect to the expres
sion of complement-regulating molecules. Pulmonary polymorphonuclear neutro
phils of the control group showed analogous changes, compared to systemic n
eutrophils, but a significantly higher rate of apoptosis and a lower increa
se of activation-marker expression were found, compared to pulmonary neutro
phils of patients with pneumonia.
Conclusions: Pulmonary neutrophils from patients with CAP show a decreased
rate of apoptosis and increased activation status in the alveolar compartme
nt, which may be important for effective control of pulmonary inflammation.