LFA-1 Deficiency Affected The Tumor Metastasis Of Lung

The process of tumor invasion and metastasis has been plagued by scientists, the tumor through the blood into the lungs, lung metastasis formation process, has been the focus of research. LFA-1 is a member of integrin family expression in leukocytes in the leukocyte adhesion, vascular endothelial cells and antigen presenting cells play a key role. The study found that the combination of white cells of LFA-1 and ICAM-1 in the tumor cells, cytotoxic lymphocytes can kill tumor cells adhesion in the occurrence and development of tumor, monitoring. But no report, LFA-1 tumor cells in the process of metastasis to the lungs in the missing will cause what kind of results. In order to study the deletion of LFA-1 gene will affect the occurrence and development of tumor, LFA-1 gene knockout mice were used as experimental group, with the background of C57 rats as control group.Research in the experimental group and the control group of mice under physiological conditions the blood routine test, in which the number of the experimental group increased by 3 times of lymphocytes, neutrophils increased trend. Research on their lung tissue under the microscope, the pulmonary septal expression in the experimental group decreased and CD45 RO protein labeled white blood cells increased significantly. We suggest that the change in the number of white blood cells, and lung tissue structure changes can affect the growth and metastasis of tumor.Therefore, using the B16F10 mouse melanoma cell line, build the tail vein injection of tumor cells after 20 days of classic, get the tumor in the lung metastasis of tumor disease model. The results showed that, the number of lung metastases were the experimental groups were increased, and the survival rate was also significantly decreased. To observe the pathological process of tumor metastasis of tumor bearing, the number and size of two groups were fifth and tenth days of lung tumor, the gross observation and microscopic observation results showed no significant differences; the fifteenth day, the mice of the experimental group increased the number of lung pulmonary tumor nodules were observed in the general conditions, and tumor volume increased; under the microscope, the malignant degree of tumor cell invasion, appeared the phenomenon. Immunohistochemical detection of Ki67 protein in lung tissue of the proliferation of the experimental group, the proliferation of tumor cells in each process point ratios are significantly up-regulated. On the fifteenth day of tumor process, the experimental group CD31 in tumor markers of angiogenesis and CD68 protein were significantly high expression of macrophage markers of immune; group while observing the tumor invasion related MMP2 and MMP9 protein were significantly up-regulated. According to the experimental results and the expression of LFA-1 in white blood cells suggests that we may, in the experimental group is the change of the tumor immune response and lung tissue of the tumor microenvironment by speeding up the process of tumor metastasis.Therefore, to explore the immune cells in mice blood, spleen and lung cancer results in fifteenth days of tumor bearing F4/80+ mice of the experimental group: in the spleen cell ratio was significantly increased; the ratio of CD8+T cells in tumor tissue decreased significantly; at the same time, in the tumor expression of secreted protein IL-17 A and IFN- y significant increase showed that the experimental group mice; immune surveillance and destruction has accelerated the process of tumor decreased in the experimental group. Research of lung tumor micro environment, the expression of IL-2, IL-10, IL-12, IL-1, TGF- beta and beta inflammatory factors such as m RNA are significantly up-regulated; among them, IL-1 beta increased more than 30 times the most significant, suggesting that we may be the main influence factor. Detection of serum in experimental group IL-1 beta was raised 2 times; enhancement can promote tumor colony formation and adherent ability. Detection of IL-1 beta protein can promote the migration and invasion of melanoma cells, joined the anti-IL-1 beta protein, reverse the results. According to the literature, IL-1 beta by up regulating the expression of tumor cell p-p38 and the up regulation of p-cjun has been confirmed.In order to study the deletion of the LFA-1 gene in mice and tumor cells by tail vein injection of lung metastasis model of system. To clarify the physiological conditions, LFA-1 gene deletion in mice can cause lung after the number of white blood cells increased; the spleen of tumor bearing mice IL-17 A and INF- gamma increases; the tumor CD8+T cells down regulated expression of LFA-1 gene deletion; will cause the lungs of mice in the micro environment of IL-1 beta, and up regulation of tumor cell p-p38 and the expression of p-cjun, and promote tumor cell proliferation, invasion and metastasis.