INTRODUCTION: Spaceflight is associated with changes in several immune parameters. Studies in rodents and humans have shown a decrease in resistance to bacterial and viral infections. However, the effect of spaceflight conditions on tumor immunity has not been explored. METHODS: The hindlimb unloading (HU) murine model of spaceflight was used to assess growth and immune reactivity to the S1 509a tumor cell line during HU as a model of microgravity. Changes in splenic mass of mice in the HU model were compared with mice in orthostatic suspension and standard housing controls. Furthermore, the role of host immunity in these changes was confirmed using mice with the severe combined immunodeficiency (SCID) mutation. RESULTS: Mice in the HU model demonstrated significantly increased tumor growth (p < 0.01), greater splenic atrophy, and a significantly diminished delayed-type hypersensitivity response to tumor antigens (p < 0.05) compared with controls. However, when immunodeficient mice were employed, no difference in tumor growth was observed. DISCUSSION: Our findings suggest antitumor immunity is inhibited in antiorthostatic suspension. The lack of a difference in mean tumor size in SCID mice in antiorthostatic suspension compared with standard housing controls supports the concept that HU alters host immunity against the S1 509a tumor. Further studies are warrranted to delineate the precise effects of spaceflight on host immunity, carcinogenesis, and tumor progression.
INTRODUCTION: Spaceflight is associated with changes in several immune parameters. Studies in rodents and humans have shown a decrease in resistance to bacterial and viral infections. However, the effect of spaceflight conditions on tumor immunity has not been explored. METHODS: The hindlimb unloading (HU) murine model of spaceflight was used to assess growth and immune reactivity to the S1 509a tumor cell line during HU as a model of microgravity. Changes in splenic mass of mice in the HU model were compared with mice in orthostatic suspension and standard housing controls. Furthermore, the role of host immunity in these changes was confirmed using mice with the severe combined immunodeficiency (SCID) mutation. RESULTS:Mice in the HU model demonstrated significantly increased tumor growth (p < 0.01), greater splenic atrophy, and a significantly diminished delayed-type hypersensitivity response to tumor antigens (p < 0.05) compared with controls. However, when immunodeficientmice were employed, no difference in tumor growth was observed. DISCUSSION: Our findings suggest antitumor immunity is inhibited in antiorthostatic suspension. The lack of a difference in mean tumor size in SCIDmice in antiorthostatic suspension compared with standard housing controls supports the concept that HU alters host immunity against the S1 509a tumor. Further studies are warrranted to delineate the precise effects of spaceflight on host immunity, carcinogenesis, and tumor progression.
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NASA Discipline Cell Biotechnology; Non-NASA Center
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