Small sputum macrophages represent highly active cells that increase in the airways of patients with inflammatory diseases such as
chronic obstructive pulmonary disease (
COPD). It has been reported often that levels of
cytokines,
chemokines and pro-teases are increased in sputum supernatants of these patients. In
COPD, the small sputum macrophages may contribute to these supernatant
proteins and recruit additional cells via specific
chemokine expression patterns. We therefore investigated the expression profile of
chemokines in sputum macrophages obtained from
COPD patients in comparison to cells from healthy donors and cells isolated after inhalation of
lipopolysaccharide (LPS). We used the minimally invasive procedure of sputum induction and have purified macrophages with the RosetteSep technology. Using macrophage purification and flow cytometry we show that in
COPD small sputum macrophages account for 85.9% ± 8.3% compared with 12.9% ± 7.1% of total macrophages in control donors. When looking at
chemokine expression we found, for the small macrophages in
COPD, increased transcript and
protein levels for CCL2, CCL7, CCL13 and CCL22 with a more than 100-fold increase for CCL13
mRNA (P < 0.001). Looking at active smokers without
COPD, there is a substantial increase of small macrophages to 60% ± 15% and, here,
chemokine expression is increased as well. In a model of airway
inflammation healthy volunteers inhaled 20 μg of
lipopolysaccharide (LPS), which resulted in an increase of small sputum macrophages from 18% ± 19% to 64% ± 25%. The pattern of
chemokine expression was, however, different with an upregulation for CCL2 and CCL7, while CCL13 was downregulated three-fold in the LPS-induced small macrophages. These data demonstrate that sputum macrophages in
COPD show induction of a specific set of CCL
chemokines, which is distinct from what can be induced by LPS.