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 establis...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.展开更多
Gastric carcinoma(GC) develops in only 1%-3% of Helicobacter pylori(H. pylori) infected people. The role in GC formation of the bacterial genotypes, gene polymorphisms and host's factors may therefore be important...Gastric carcinoma(GC) develops in only 1%-3% of Helicobacter pylori(H. pylori) infected people. The role in GC formation of the bacterial genotypes, gene polymorphisms and host's factors may therefore be important. The risk of GC is enhanced when individuals are infected by strains expressing the oncoprotein CagA, in particular if CagA has a high number of repeats containing the EPIYA sequence in its C'-terminal variable region or particular amino acid sequences flank the EPIYA motifs. H. pylori infection triggers an inflammatory response characterised by an increased secretion of some chemokines by immunocytes and colonised gastric epithelial cells; these molecules are especially constituted by proteins composing the interleukin-1beta(IL-1β) group and tumour necrosis factor-alpha(TNF-α). Polymorphisms in the promoter regions of genes encoding these molecules, could account for high concentrations of IL-1β and TNF-α in the gastric mucosa, which may cause hypochlorhydria and eventually GC. Inconsistent results have been attained with other haplotypes of inflammatory and anti-inflammatory cytokines. Genomic mechanisms of GC development are mainly based on chromosomal or microsatellite instability(MSI) and deregulation of signalling transduction pathways. H. pylori infection may induce DNA instability and breaks of double-strand DNA in gastric mucocytes. Different H. pylori strains seem to differently increase the risk of cancer development run by the host. Certain H. pylori genotypes(such as the cagA positive) induce high degrees of chronic inflammation and determine an increase of mutagenesis rate, oxidative-stress, mismatch repair mechanisms, down-regulation of base excision and genetic instability, as well as generation of reactive oxygen species that modulate apoptosis; these phenomena may end to trigger or concur to GC development.展开更多
基金Supported by a grant from the Chios Gum Mastic Growers Association
文摘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.
文摘Gastric carcinoma(GC) develops in only 1%-3% of Helicobacter pylori(H. pylori) infected people. The role in GC formation of the bacterial genotypes, gene polymorphisms and host's factors may therefore be important. The risk of GC is enhanced when individuals are infected by strains expressing the oncoprotein CagA, in particular if CagA has a high number of repeats containing the EPIYA sequence in its C'-terminal variable region or particular amino acid sequences flank the EPIYA motifs. H. pylori infection triggers an inflammatory response characterised by an increased secretion of some chemokines by immunocytes and colonised gastric epithelial cells; these molecules are especially constituted by proteins composing the interleukin-1beta(IL-1β) group and tumour necrosis factor-alpha(TNF-α). Polymorphisms in the promoter regions of genes encoding these molecules, could account for high concentrations of IL-1β and TNF-α in the gastric mucosa, which may cause hypochlorhydria and eventually GC. Inconsistent results have been attained with other haplotypes of inflammatory and anti-inflammatory cytokines. Genomic mechanisms of GC development are mainly based on chromosomal or microsatellite instability(MSI) and deregulation of signalling transduction pathways. H. pylori infection may induce DNA instability and breaks of double-strand DNA in gastric mucocytes. Different H. pylori strains seem to differently increase the risk of cancer development run by the host. Certain H. pylori genotypes(such as the cagA positive) induce high degrees of chronic inflammation and determine an increase of mutagenesis rate, oxidative-stress, mismatch repair mechanisms, down-regulation of base excision and genetic instability, as well as generation of reactive oxygen species that modulate apoptosis; these phenomena may end to trigger or concur to GC development.
