Trefa Mohammed Abdullah
Abstract
Background: Antitumor-targeting drugs can stimulate dendritic cells (DCs) indirectly through the shedding of dying tumor cells as part of what is referred to as a “danger signal”. Although chemotherapeutic agents have been shown to kill dendritic cells (DCs), the effects of low, non-cytotoxic ...
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Background: Antitumor-targeting drugs can stimulate dendritic cells (DCs) indirectly through the shedding of dying tumor cells as part of what is referred to as a “danger signal”. Although chemotherapeutic agents have been shown to kill dendritic cells (DCs), the effects of low, non-cytotoxic doses on DC function have not been studied.Objective: To investigate the impact of various concentrations of mitomycin C at low, non-cytotoxic doses on the maturation of DCs.Material and Methods: THP-1 monocytes were differentiated into immature dendritic cells using IL-4 and GM-CSF. HCT116 colorectal cancer cells were treated with mitomycin C at concentrations ranging from 10 to 80 nM and co-cultured with undifferentiated dendritic cells. The expression of co-stimulatory molecules (CD11c, CD80, CD83, CD86, HLA-DR, CD14) and IL-12p70 secretion were measured.Results: Different dosages of Mitomycin C-treated HCT116 cells enhanced the maturation of dendritic cell markers (CD80, CD83, CD86, HLA-DR), but reduced CD14 levels (p< 0.01). While increasing the Mitomycin C dose to 80 nM further upregulated HLA-DR and CD86 expression, the release of IL-12 was highest a 50 nM concentration of mitomycin C (686.7 ± 125.7 pg/mL compared to 263.8 ± 4.8 pg/mL in controls; p < 0.05). IL-12 levels were not significantly increased even with 30 nM Mitomycin C.Conclusion: Low concentrations of Mitomycin C contributed to an increase in dendritic cellmaturation and an increase in the expression of co-stimulatory molecules (CD80, CD86, CD83, and HLA-DR), along with the secretion of cytokines such as IL-12p70, IL-2, and GM-CSF.
Ali Asghar Ebrahimi; Hamid Noshad; Shahram Sadreddini; Mohammad Saeid Hejazi; Yashar Mohammadzadeh Sadigh; Yashar Eshraghi; Morteza Ghojazadeh
Abstract
Background: Rheumatoid arthritis (RA) is a chronic multisystem autoimmune disease common in all races and ethnics. Cytokines and cytokines receptors play an important role in RA pathogenesis and clinical presentation. Objective: To investigate the serum levels of TNF-α, TNF-α RI, TNF-α ...
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Background: Rheumatoid arthritis (RA) is a chronic multisystem autoimmune disease common in all races and ethnics. Cytokines and cytokines receptors play an important role in RA pathogenesis and clinical presentation. Objective: To investigate the serum levels of TNF-α, TNF-α RI, TNF-α RII and IL-12 in RA patients and healthy control group. Methods: In this study 43 patients fulfilling the revised criteria of American College of Rheumatology (ACR) for RA and 13 healthy cases as a control group were selected for TNF-α, TNF-αRI, TNF-αRII and IL-12 serum level analysis. The patients' age was 42.2 ± 22 and the age of healthy group was 40.1 ± 19.2 years (p=0.1). The pa-tients had an active disease with at least six swollen and ten tender joints. Minimum ESR was 28 mm at first hours of the morning. Early morning stiffness in patients lasted longer than 45 minutes. Results: Our study showed that IL-12 serum level of the pa-tients (91.69 ± 43.07 ρg/ml) and control (61.79 ± 40.08 ρg/ml) group was significantly different (p<0.001). The serum level of TNF-αRI was 2.36 ± 0.77 ng/ml in the patient and 1.73 ± 0.37 ng/ml in the control group (p<0.01). TNF-αRII serum concentration in patients was 8.89 ± 2.3 ng/ml, while that of control group was 7.06±1.30 ng/ml (p=0.03). The serum level of TNF-α in patients was 32.90 ± 19.27 ρg/ml and that of the control group was 24.27± 8.28 ρg/ml (p=0.08) with no significant difference between the two. Conclusions: It is concluded that IL-12, TNF-αRI and TNF- αRII serum con-centrations are more important and better predictive factors than TNF-α in RA course and in the active forms of the disease.
Kazem Ahmadi; Majid Riazipour
Abstract
Background: The water-soluble extract of Ganoderma lucidum (Reishi) has been used as an immunomodulator to stimulate spleen cells proliferation and cytokine expression. Objective: To investigate the effect of Ganoderma lucidum (G. lucidum) on cytokine production by mice peritoneal macrophages. Methods: ...
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Background: The water-soluble extract of Ganoderma lucidum (Reishi) has been used as an immunomodulator to stimulate spleen cells proliferation and cytokine expression. Objective: To investigate the effect of Ganoderma lucidum (G. lucidum) on cytokine production by mice peritoneal macrophages. Methods: Mice peritoneal macrophages were prepared by intra-peritoneal injection of 5 ml cold PBS. Peritoneal macrophages were plated out at 1X106 cell/well in 1ml RPMI 1640 medium supplemented with 10%FCS, 50 μg streptomycin and 50U penicillin. Cells were incubated in the presence or absence of different concentrations of G. lucidum at 370C and 5% CO2 for 48 hours. Cell free medium was removed and used for cytokine assay by ELISA method (Bender med system). Results: The results showed no significant differences in cell viability at concentrations ranged from 0-40 μg/ml compared with control group. G. lucidum enhanced IL-1β, TNF-α and NO production in a concentration dependent manner. However, it is not clear if the enhancement of NO release is due to direct effect of G. lucidum on NO synthesis or by indirect endogenous modulation via cytokines. IL-12 release by peritoneal macrophages was also increased in response to different concentrations of G. lucidum, but maximum enhancement was induced in response to 5 μg/ml of G. lucidum (p<0.001). Conclusion: Our results indicate that G. lucidum at concentrations used has a positive effect on cytokine release and NO production by peritoneal macrophages. Therefore, it is concluded that G. lucidum at moderate concentrations improves macrophage function through cytokine and NO release.
