Immunological mechanism of low-dose priming radiation resistance in walker-256 tumor model mice

Abstract

Abstract. The aim of the present study was to investigate whether low-dose priming radiation induces antitumor immunity that can be augmented by the modulation of natural killer (NK) cell and cytokine activity using a mouse tumor model. Walker-256 cells were injected into the right flank of male BALB/c mice. At 7 days after inoculation, mice were divided into three groups, including group 1,2,3. In group 1 the mice were without radiation, in group 2 the mice were received 2 Gy radiation only, and in group 3 the mice were radiated with a priming dose of 75 mGy followed by 2 Gy radiation after 24 h. On day 21 following the radiation, the tumors were removed and the tumor index (tumor weight as a percentage of body weight) was calculated. At 1, 7, 14 and 21 days following the 2 Gy radiation, mouse splenocytes were isolated to analyze the NK activity and measure the production of the cytokines interleukin-1β, interferon-γ and tumor necrosis factor-α by ELISA. Apoptosis was also measured by flow cytometry. The results demonstrated that priming radiation significantly delayed the tumor growth and prolonged the median survival time to 38 days compared with the 31-day survival in the 2 Gy radiation group. The percentage of apoptotic cells was significantly higher in the mice that received 75 mGy + 2 Gy radiation compared with that in the mice that received 2 Gy alone; by contrast, mice that were not irradiated exhibited a relatively low level of apoptosis. The primed mice had a higher level of NK activity as compared with the mice exposed to 2 Gy radiation only or mice that were not irradiated. Furthermore, cytokine expression remained at a higher level in mice receiving priming dose of radiation compared that in the mice receiving only 2 Gy radiation. In conclusion, the results indicated that low-dose priming X-ray radiation may enhance the NK activity and the levels of cytokines, and that the immune response serves an important role in anticancer therapy, including radiotherapy.

Preliminary Results of the Effects of Localized High-Dose Radiotherapy Combined with Total Body Low-Dose Irradiation on Tumor Growth and Stimulating the Immune System in Tumor-Bearing Mice

“…It may imply that TB+LH enhanced the immune system more efficiently and consequently resulted in a higher tumor volume reduction and increased lifespan. Feng et al [16] irradiated the mice with 75 mGy priming electron rays, and 24 h later irradiated the tumors previously injected into the flank of the mice with 2 Gy X-rays. They also irradiated another group of mice with only 2 Gy localized irradiation.…”

“…Feng et al [ 16 ] irradiated the mice with 75 mGy priming electron rays, and 24 h later irradiated the tumors previously injected into the flank of the mice with 2 Gy X-rays. They also irradiated another group of mice with only 2 Gy localized irradiation.…”

Exploring the optimal dose of low ionizing radiation to enhance immune function: a rabbit model

“…Animal experiment reagents and instruments included depilatory cream (sodium sulfide and the distilled water 1:9), 75% ethanol solution, 1.5% pentobarbital sodium, 3% pentobarbital sodium, Anerdian, 0.9% isotonic saline, penicillin, 3 VX-2 tumor tissue (provided by the Fourth Affiliated Hospital of Harbin Medical University, Harbin, China), enzyme-linked immunosorbent assay (ELISA) kits (Shanghai Future Industrial Co. Ltd., Shanghai, China), microplate reader, centrifuges, incubator, digital color ultrasonic diagnostic instrument (Feiyinuo Technology Co. Ltd., Suzhou, China), Varian linac IX, slicing machine, optical microscope, and automatic hemocyte analyzer.…”

“…Tumor biotherapy is the application of biological technologies or biological agents to regulate the body’s autoimmune response and achieve tumor suppression. 3 Tumor immunotherapy can improve immune function while killing tumor cells in vivo . A previous study found that the combination of traditional treatment and immunotherapy is better than single treatment, and it also provides a theoretical reference for future clinical treatment.…”

Evidence of Nrf2/Keap1 Signaling Regulation by Mitochondria-Generated Reactive Oxygen Species in RGK1 Cells

“…It is known that in chemotherapy, once cancer cells have been exposed to a drug, they become resistant to further treatment [ 17 ]. Similarly, after cells are dosed with radiation, they become resistant to further doses [ 18 , 19 ]. These phenomena may explain cells responding to severe oxidative stress and must repeatedly respond subsequently to a series of oxidative insults.…”