Study objectives: 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.
Design and 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.
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.