• Shin-ichiro Takeda, Toru Sato, Tatsuro Katsuno, Tomoo Nakagawa, Yoshiko Noguchi, Osamu Yokosuka, and Yasushi Saito.
• Department of Clinical Cell Biology, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba-shi, Japan.
• Dig. Dis. Sci. 2010 Jul 1;55(7):1886-95.

BackgroundTwo main functionally distinct monocytes phenotypes are known: the CD14(hi)CD16(-) "classical" and the CD14(+)CD16(+) "proinflammatory" phenotypes. The latter phenotype is elevated in patients with ulcerative colitis (UC) and is suspected to have a major role in the immunopathogenesis of UC.AimTo selectively deplete circulating proinflammatory CD14(+)CD16(+) monocyte phenotype.MethodsSeven corticosteroid-naïve patients with UC (clinical activity index = 8.7 +/- 1.3) and seven healthy subjects were included. In patients with UC, granulocyte/monocyte adsorption (GMA) was done with an Adacolumn that selectively adsorbs leucocytes of the myeloid lineage. Blood from all subjects at baseline and from the patients immediately after the first GMA session was processed. Isolated monocytes were subjected to fluorescence-activated cell sorter analyses.ResultsThe seven UC patients achieved remission (CAI ConclusionsWe found high expressions of alpha4 integrin and CX(3)CR1 on monocytes in patients with active UC, known to promote the extravasation of CD14(+)CD16(+) monocytes into the mucosa. GMA effectively depletes CD14(+)CD16(+) monocytes and concomitantly increases CD14(hi)CD16(-)CCR2(low) "immature" monocytes; thus GMA was associated with the emergence of less inflammatory monocyte phenotype in circulation.

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