Effect of 50-Hz magnetic fields on the expression of activation-induced deaminase, B-cell lymphoma 6 and serum levels of interleukin-6, interleukin-21.

BACKGROUND: Investigations showed different effects of magnetic fields (MFs) on the immune system. During humoral immune responses, genes of activation-induced deaminase (AID) and B-cell lymphoma-6 (Bcl-6) are expressed and interleukin (IL)-6 and IL-21 are produced. These factors play significant roles in class switching, affinity maturation of antibodies and activations of B cells germinal centers (GCs). Therefore, this study investigated the effect of 50-Hz MFs exposure with different densities on these factors. MATERIALS AND METHODS: Eighty rats were divided into four exposures and control groups. The treatment groups were exposed to magnetic flux densities of 1, 100, 500, and 2000 µT (50 Hz, 2 h/d for 60 d). To activation of the immune system, all the animals were immunized with human serum albumin on days 31, 44, and 58 of exposure. Reverse transcription-quantitative polymerase chain reaction was used to assay the expression levels of AID and Bcl-6 genes in the spleen. The serum levels of IL-6 and IL-21 were also detected by enzyme-linked immunosorbent assay at the pre-and post-immunization phases. RESULTS: AID expression was significantly declined at 1µT magnetic flux density, while no change was observed in the expression of Bcl-6. Serum IL-6 was increased only in the 500 µT group at the post-immunization phase. CONCLUSIONS: It seems exposure to 50-Hz MFs at 1 µT density, suppresses AID and may cause a decline in class switching and affinity maturation of Abs. On the other hand, exposure to 500 µT, may activate them. These findings demonstrate the various potential effects of MFs on the humoral immune system.

Impact of interleukin-32α on T helper cell-related cytokines, transcription factors, and proliferation in patients with type 2 diabetes mellitus.

OBJECTIVE: The ability of interleukin (IL)-32α to induce T helper (Th) 1, Th17, and Treg cytokines (interferon gamma [IFN-γ], IL-17, and IL-10, respectively), and transcription factors ([signal transducer and activator of transcription (STAT) 1 and T-box (T-bet) for Th1, STAT3 and retinoid-related orphan receptor (ROR)-γt for Th17, and STAT5 and forkhead box P3 (Foxp3) for Treg]) were investigated in type 2 diabetes mellitus (T2DM). IL-32α effects on Th cell proliferation and related factors including IL-2 and NF-κB were also explored. METHODS: Serum levels of IL-32α in 31 patients and 31 healthy controls (HCs) were determined by ELISA assay. CD4+ T cells cultured with polyclonal activators in the presence and absence of recombinant IL-32α (rIL-32α). Gene expressions in cultured Th cells were assessed with real-time PCR. Cytokines in supernatants were measured with ELISA. Proliferation experiments were assessed by flow cytometry. RESULTS: The patients showed significant increase in IL-32α levels compared with HCs and its levels were positively correlated with fasting plasma glucose (FPG) and hemoglobin A1c (HbA1c). rIL-32α enhanced IL-17 and IL-2 production, increased ROR-γt and NF-κB expression, and enhanced Th proliferation in both patients and HCs. In patients, IL-17, ROR-γt, NF-κB, and proliferation levels were higher than those in HCs, in cultures with and without rIL-32α (rIL-32α+ and rIL-32α-). IL-2 levels in rIL-32α+cultures of patients were significantly higher than the HCs, and it was positively correlated with proliferation rate and NF-κB expression. CONCLUSIONS: Aberrant IL-32α levels are participated in T2DM pathogenesis. IL-32α potently induces Th17-related factors and amplifies the proliferative function of T cells.HighlightsEnhanced serum levels of IL-32α in T2DM patients was correlated with FPG and HbA1c.IL-32α increases ROR-γt expression and IL-17 production, and induces Th17 cells.IL-32α enhances NF-κB expression and IL-2 production, and promotes Th proliferation.IL-32α is more effective for inducing Th17 cells and proliferation in the patients.IL-32α axis could be mentioned as a future therapeutic goal for the T2DM.

Effect of 50-Hz Magnetic Fields on Serum IL-1ß and IL-23 and Expression of BLIMP-1, XBP-1, and IRF-4.

Investigations demonstrated that magnetic fields (MFs) change cytokine production and expression of some immune system genes. This alteration can affect the immune system function and may lead to some diseases. Therefore, this study investigated two important inflammatory cytokines, i.e., IL-1ß and IL-23 at two phases of pre- and post-immunization of the immune system. In addition, the expressions of three important genes in the humoral immunity, i.e., B lymphocyte-induced maturation protein-1 (BLIMP-1), X-box-binding protein-1 (XBP-1), and interferon regulatory factor-4 (IRF-4) were evaluated at post-immunization phase. Eighty adult male rats were divided into four experimental groups and a control. The experimental groups were exposed to 50 -Hz MFs with magnetic flux densities of 1, 100, 500, and 2000 µT, 2 h/day for 2 months. The animals were injected by human serum albumin (100 µg/rat) on days 31, 44, and 58 of exposure. The cytokine levels in serum were measured with enzyme-linked immunosorbent assay (ELISA), and the expression of genes was evaluated with reverse transcription quantitative polymerase chain reaction (RT-qPCR). Serum IL-1ß was decreased at pre-immunization phase after exposure to 1 and 100 µT of 50-Hz MFs. In contrast, serum IL-23 was increased at post-immunization phase in 100 µT group. No change was observed in serum IL-1ß and IL-23 in each group at pre-immunization phase compared with post-immunization. Furthermore, exposure to 100 µT downregulated expression of BLIMP-1, XBP-1, and IRF-4. In conclusion, exposure to 50-Hz MFs may decrease inflammation at short time and increase it at longer time exposures. In addition, 50-Hz MF exposure may decrease the humoral immune responses. It seems that 50-Hz MFs cause more alteration in immune system function at lower densities (100 µT).