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Lymphatic Pump Treatment Increases Leukocyte Trafficking and Inhibits Tumor Formation in the Lungs of Rats

Journal: The Journal of the American Osteopathic Association Date: 2010/08, 110(8):Pages: 478. doi: Subito , type of study: animal experiment

Full text    (https://www.degruyter.com/document/doi/10.7556/jaoa.2010.110.8.445/html)

Keywords:

animal experiment [67]
immune response [11]
leukocytes [9]
LPT [27]
lung [38]
lymph flow [4]
lymphatic pump technique [43]
tumor [15]

Abstract:

Introduction: Immune responses play a vital role in the development and metastasis of tumors. Studies from our laboratory demonstrate that lymphatic pump treatment (LPT) increases lymph flow and mobilizes leukocytes into lymphatic circulation in both dogs and rats. In addition to the direct effects of increased numbers of circulating leukocytes produced by LPT, it seems likely that these cells improve immune surveillance, which may enhance protection against tumor development and metastasis. Hypothesis: Lymphatic pump treatment enhances antitumor immunity and reduces solid tumors in the lungs of rats. Methods: F344 rats were injected intravenously with MADB106, a commonly used cancer cell line that forms solid tumors in the lungs of rats. Twenty-four hours following tumor injection, rats received no treatment (control), 4 minutes of light touch under anesthesia (sham), or 4 minutes of LPT under anesthesia, for 7 consecutive days. Eight days after tumor injection, tissues were removed and measured for solid tumors, leukocyte populations, immune cell activity, and lysis of tumors. Serum and lung fluid was measured for vascular endothelial growth factor C (VEGF-C), a biomarker for lymphangiogenesis. Results: Lymphatic pump treatment significantly (P<.05) reduced solid tumors in the lungs compared to control and sham treatment. In addition, LPT significantly (P<.05) increased the numbers of B cells, CD4+ T cells, CD8+ T cells, NK cells, and macrophages in the lungs. There were no differences in the levels of VEGF-C between treatment groups, suggesting that LPT does not promote lymphangiogenesis during the early stages of tumor development. Finally, to measure antitumor immune responses, leukocytes were isolated from the lungs and spleen and cultured with tumors in vitro. There were no differences in tumor specific cytokine production or tumor lysis between treatment groups, suggesting that LPT does not enhance leukocyte activities in vitro. Conclusion: Our data suggest LPT inhibits pulmonary tumor formation by enhancing the numbers of leukocytes with antitumor activities that migrate into the lungs. The results from this study provide scientific support for the clinical use of LPT to enhance antitumor immunity.


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