Effects of microgravity and other space stressors in immunosuppression and viral reactivation with potential nervous system involvement.

Space exploration exposes astronauts to a variety of gravitational stresses. Exposure to a reduced gravity environment affects human anatomy and physiology. Countermeasures to restore homeostatic states within the human body have begun. The pathophysiological effects of exposure to microgravity, on the neurological system, are, however, still not clear. NASA has scheduled deep space exploration of extraterrestrial locations such as the Moon and Mars in the 2030s. Adverse health effects related to the human exposure to microgravity from previous, relatively shorter missions have been documented. A lengthy deep space travel to Mars could be overburdened by significant adverse health effects. Astronauts demonstrate a significant increase in the number of many types of circulating white blood cells (neutrophils, monocytes, T-helper cells, and B-cells) but a decrease in natural killer cells. It is unclear whether these changes are due to increased production or decreased clearance of these cells. In this review, viral reactivation in astronauts will be discussed, including the occurrence of clinical cases before, during, or after spaceflight and their management during and after flight. Studies on models used in spaceflight studies such as the AKATA cells (an immortalized B-cell line derived from a Japanese patient with Burkitt's lymphoma, a tumor induced by Epstein-Barr virus) and other cell lines which shed these latent viruses, will be reviewed with specific reference to gravitational changes, radiation, and spaceflight-induced immune suppression.

Active hexose correlated compound modulates LPS-induced hypotension and gut injury in rats.

We hypothesized that AHCC; (Amino UP Chemical Co., Ltd., Sapporo, Japan), a mushroom mycelium extract obtained from liquid culture of Lentinula edodes, restores immune function in LPS-induced inflammation in the gut, especially when the nitric oxide signaling pathway is impaired. This is the first inter-disciplinary proposal to identify molecular mechanisms involved in LPS-induced immune dysfunction in the gut in conscious animals treated or non-treated with AHCC, a promoter of immune support. Specifically, we have tested the effects of AHCC on LPS-induced deleterious effects on blood pressure and gut injury in conscious rats. The time course of biological markers of innate/acquired immune responses, and inflammation/oxidative stress is fully described in the present manuscript. Rats were randomly assigned into 3 groups (N=6 per group). Group 1 received 10% of AHCC in drinking water for 5days; Group 2 received lipopolysaccharide (LPS; Escherichia coli 0111:B4 purchased from Sigma) only at 20mg/kg IV; Group 3 received combined treatments (AHCC + LPS). LPS was administered at 20mg/kg IV, 5days following AHCC treatment. We have demonstrated that AHCC decreased the LPS-deleterious effects of blood pressure and also decreased inflammatory markers e.g., cytokines, nitric oxide and edema formation. Finally, AHCC diminished lymphocyte infiltration, restoring gut architecture. Because AHCC was administered prior to LPS, our results indicate the potential impact of AHCC's prophylactic effects on LPS inflammation. Consequently, additional experiments are warrant to assess its therapeutic effects in sepsis-induced inflammation.