Suppression of Inflammatory Cytokine Secretion by Granulocyte/Monocyte Adsorptive Apheresis in Active Ulcerative Colitis

<jats:p><jats:bold>Abstract: </jats:bold> To elucidate the molecular mechanisms involved in the therapeutic effects of granulocyte/monocyte adsorption apheresis, changes were investigated in the cytokine responses of peripheral blood mononuclear cells (PBMC) before and after granulocyte/monocyte adsorptive apheresis in ulcerative colitis (UC) patients. Four patients with active UC were enrolled. All patients responded to granulocyte/monocyte adsorptive apheresis. A total of 20 sessions of four patients were analyzed. Peripheral blood mononuclear cells were isolated from peripheral venous blood within 5 min before and after each session of granulocyte/monocyte adsorptive apheresis. The cells were stimulated with interleukin (IL)‐1β and tumor necrosis factor (TNF)‐α for 24 h, and the secreted IL‐8 and IL‐6 levels were determined by enzyme‐linked immunosorbent assay (ELISA). IL‐1β‐induced IL‐8 and IL‐6 secretion was significantly decreased after granulocyte/monocyte adsorptive apheresis. TNF‐α‐induced IL‐8 secretion was also significantly decreased after apheresis, but there was no significant difference in TNF‐α‐induced IL‐6 secretion (<jats:italic>P</jats:italic> = 0.052). In conclusion, granulocyte/monocyte adsorptive apheresis down‐regulates the IL‐1β‐ and TNF‐α‐induced inflammatory responses in PBMC. The induction of hyporesponsiveness to pro‐inflammatory cytokines may be an important factor mediating the clinical effects of granulocyte/macrophage adsorptive apheresis in UC patients.</jats:p>