The Immune System in Space, Including Earth-Based Benefits of Space- Based Research

Abstract

Exposure to space flight conditions has been shown to result in alterations in immune responses. Changes in immune responses of humans and experimental animals have been shown to be altered during and after space flight of humans and experimental animals or cell cultures of lymphoid cells. Exposure of subjects to ground-based models of space flight conditions, such as hindlimb unloading of rodents or chronic bed rest of humans, has also resulted in changes in the immune system. The relationship of these changes to compromised resistance to infection or tumors in space flight has not been fully established, but results from model systems suggest that alterations in the immune system that occur in space flight conditions may be related to decreases in resistance to infection. The establishment of such a relationship could lead to the development of countermeasures that could prevent or ameliorate any compromises in resistance to infection resulting from exposure to space flight conditions. An understanding of the mechanisms of space flight conditions effects on the immune response and development of countermeasures to prevent them could contribute to the development of treatments for compromised immunity on earth.

Osteopontin: Role in immune regulation and stress responses

“…As compared to chronic restraint stress, mice experiencing hind limb-unloading have free access to food and water and thus are not affected by starvation and dehydration whereas CRS is a more psychological stressor. Exposure to HU causes alterations in the immune system, including organ atrophy, similar to those observed after space flight (Sonnenfeld, 2005). Wei and colleagues (Wei et al, 2003) demonstrated that HU causes a dramatic reduction in the number of mouse splenocytes and thymocytes; the reduction in lymphocyte number resulting from stress is corticosteroid-dependent and apparently due to the induction of apoptosis.…”

“…restraint, hindlimb unloading, stroke and microgravity) can cause the involution of the spleen and/or thymus, thus impairing the organism's ability to mount an immune response (Sonnenfeld, 2005;Dhabhar et al, 1995;Marcucci et al, 1980). The loss of spleen and thymus cellularity could be caused by one or a combination of factors, including increased cell death, reduced proliferation capacity in response to mitogenic stimulation, and redistribution of the lymphocytes in the body (Dhabhar et al, 1995).…”

“…The 3-day HU model not only mimics microgravity as experienced by astronauts in space flight but also imposes great physical challenges and chronic stress on the organism. These challenges lead to rapid systemic changes in stress hormone production, immune cell distribution, and cytokine/chemokine production; they also affect peripheral immune organs in the immune system (Sonnenfeld, 2005). Although different stress paradigms have been operationally defined as "chronic physical stress", the extent to which each of these …”

Osteopontin regulates hindlimb-unloading-induced lymphoid organ atrophy and weight loss by modulating corticosteroid production

“…Compared with physicalrestraint stress, mice under HU have free access to food and water and thus are not transiently deprived of either. Exposure to HU causes alterations in the immune system, including immune organ atrophy, similar to those observed after space flight (23). Wei et al (24) demonstrated that HU caused a dramatic reduction in the number of mouse splenocytes and thymocytes; the reduction in lymphocyte number resulting from stress was corticosteroid-dependent and apparently caused by the induction of apoptosis.…”

Plasma Osteopontin Modulates Chronic Restraint Stress-Induced Thymus Atrophy by Regulating Stress Hormones: Inhibition by an Anti-Osteopontin Monoclonal Antibody

“…We have demonstrated that OPN is at least partially responsible for hind limbunloading (HU) stress-induced losses in peripheral lymphocytes and thymocytes (8). This type of stress leads to rapid systemic changes in stress hormone production, immune cell distribution, and cytokine/chemokine production; it also affects peripheral immune organs in the immune system (9). OPN-deficient mice showed significantly milder changes in response to this stress.…”