Alterations in the function of circulating mononuclear cells derived from patients with Crohn＇s disease treated with mastic

AIM： To assess the effects of mastic administration on cytokine production of circulating mononuclear cells of patients with active Crohn＇s disease （CD）. METHODS： The study was conducted in patients with established mildly to moderately active CD, attending the outpatient clinics of the hospital, and in healthy controls. Recruited to a 4 wk treatment with mastic caps （6 caps/d, 0.37 g/cap） were 10 patients and 8 controls, all of who successfully completed the protocol. Interleukin-6 （IL-6）, tumor necrosis factor-alpha （TNF-α）, monocyte chemotactic protein-1 （MCP-1）, macrophage migration inhibitory factor （MIF） and intracellular antioxidant glutathione （GSH） were evaluated in peripheral blood mononuclear cells （PBMC） before and after treatment. RESULTS： Treating CD patients with mastic resulted in the reduction of TNF-α secretion （2.1 ± 0.9 ng/mL vs 0.5 ± 0.4 ng/mL, P = 0.028）. MIF release was significantly increased （1.2±0.4 ng/mL vs 2.5 ± 0.7 ng/mL, P = 0.026） meaning that random migration and chemotaxis of monocytes/macrophages was inhibited. No significant changes were observed in IL-6, MCP-1 and GSH concentrations. CONCLUSION： This study shows that mastic acts as an immunomodulator on PBIC, acting as a TNF-α inhibitor and a MIF stimulator. Although further double-blind, placebo-controlled studies in a large number of patients is required to clarify the role of this natural product, this finding provides strong evidence that mastic might be an important regulator of immunity in CD.

Alterations in the function of circulating mononuclear cells derived from patients with Crohn's disease treated with mastic

AIM: To assess the effects of mastic administration on cytokine production of circulating mononuclear cells of patients with active Crohn's disease (CD). METHODS: The study was conducted in patients with established mildly to moderately active CD, attending the outpatient clinics of the hospital, and in healthy controls. Recruited to a 4 wk treatment with mastic caps (6 caps/d, 0.37 g/cap) were 10 patients and 8 controls, all of who successfully completed the protocol. Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), monocyte chemotactic protein-1 (MCP-1), macrophage migration inhibitory factor (MIF) and intracellular antioxidant glutathione (GSH) were evaluated in peripheral blood mononuclear cells (PBMC) before and after treatment. RESULTS: Treating CD patients with mastic resulted in the reduction of TNF-alpha secretion (2.1 +/- 0.9 ng/mL vs 0.5 +/- 0.4 ng/mL, P = 0.028). MIF release was significantly increased (1.2 +/- 0.4 ng/mL vs 2.5 +/- 0.7 ng/mL, P = 0.026) meaning that random migration and chemotaxis of monocytes/macrophages was inhibited. No significant changes were observed in IL-6, MCP-1 and GSH concentrations. CONCLUSION: This study shows that mastic acts as an immunomodulator on PBMC, acting as a TNF-alpha inhibitor and a MIF stimulator. Although further double-blind, placebo-controlled studies in a large number of patients is required to clarify the role of this natural product, this finding provides strong evidence that mastic might be an important regulator of immunity in CD.