CD4(+) T cells epigenetically modified by oxidative stress cause lupus-like autoimmunity in mice.

Lupus develops when genetically predisposed people encounter environmental agents such as UV light, silica, infections and cigarette smoke that cause oxidative stress, but how oxidative damage modifies the immune system to cause lupus flares is unknown. We previously showed that oxidizing agents decreased ERK pathway signaling in human T cells, decreased DNA methyltransferase 1 and caused demethylation and overexpression of genes similar to those from patients with active lupus. The current study tested whether oxidant-treated T cells can induce lupus in mice.

Oxidative stress, T cell DNA methylation, and lupus.

Objective: Lupus develops when genetically predisposed people encounter environmental agents, such as ultraviolet light, silica, infections, and cigarette smoke, that cause oxidative stress, but how oxidative damage modifies the immune system to cause lupus flares is unknown. We previously showed that inhibiting DNA methylation in CD4+ T cells by blocking ERK pathway signaling is sufficient to alter gene expression, and that the modified cells cause lupus-like autoimmunity in mice. We also reported that T cells from patients with active lupus have decreased ERK pathway signaling, have decreased DNA methylation, and overexpress genes normally suppressed by DNA methylation.

Trichostatin A sensitizes cisplatin-resistant A549 cells to apoptosis by up-regulating death-associated protein kinase.

Aim: To investigate the apoptosis-inducing effect of trichostatin A (TSA) in the human lung adenocarcinoma cisplatin-resistant cell line (A549/CDDP) and to examine whether TSA can enhance sensitivity to cisplatin treatment and the underlying molecular mechanisms of such an enhancement.

Methods: Cell viability was evaluated using the Neutral Red assay. Apoptosis was assessed using Hoechst 33258 staining and flow cytometry analysis.

Age-dependent decreases in DNA methyltransferase levels and low transmethylation micronutrient levels synergize to promote overexpression of genes implicated in autoimmunity and acute coronary syndromes.

T cell DNA methylation levels decline with age, activating genes such as KIR and TNFSF7 (CD70), implicated in lupus-like autoimmunity and acute coronary syndromes. The mechanisms causing age-dependent DNA demethylation are unclear. Maintenance of DNA methylation depends on DNA methyltransferase 1 (Dnmt1) and intracellular S-adenosylmethionine (SAM) levels, and is inhibited by S-adenosylhomocysteine (SAH).

[Study on immunorepressive mice model by gamma irradiation].

Objective: To establish the immunorepressive mice model by irradiation.

Methods: The 90 Kunming mice which the weight is from 30 to 34g were treated with 3Gy, 4Gy, 5Gy gamma irradiation, the delayed allergy testing, the serum haemolysin level testing, the phagocytosing functions testing and the NK cell activity testing were performed at 3th, 7th, 14th, 21th days after irradiation respectively.

Results And Conclusion: (1) All 3Gy, 4Gy, 5Gy gamma irradiation can cause mice immunorepressivestate except the NK cell activity.

[Development of methods on detection of enteropathogenic Escherichia coli by double PCR in meat and meat product].

Objective: To establish a rapid method for detecting Enteropathogenic Escherichia coli (EPEC) in meat and meat product.

Methods: Based on attaching and effacing lesion (eaeA gene) and bundle-forming pili (bfpA gene) of EPEC, two pairs of primers were designed. Then EPEC in meat and meat product were detected by double PCR.

[Clinical value of tumor supplied group of factor combined with CEA in diagnosing tuberculosis pleural effusion and malignant pleural effusion].

Objectives: To determine the clinical value of tumor supplied group of factor (TSGF) combined with carcinoembryonic antigen (CEA) in diagnosing tukerculosis pleural effusion and malignant pleurul effusion.

Methods: TSGF and CEA were detected by ELISA in 14 patients with tuberculosis pleural effusion and 28 patients with malignant pleural effusion.

Results: The average levels of TSGF and CEA in patients with malignant pleural effusion were higher than those with tuberculosis pleural effusion.