Pharmacological countermeasures to spaceflight-induced alterations of the immune system

Opportunities for microbes to establish infections are enhanced under spaceflight conditions because space travel stimulates their growth (Chap. 15) and has a negative impact on immune functions. Indeed, it has been shown that spaceflight affects lymphoid organs (Gridley et al. 2003; Baqai et al. 2009) and induces variations in peripheral blood leukocyte subsets (Chap. 9). Neutrophil, monocyte, and NK cell functions are affected by spaceflight (Chaps. 10-12). The activation of T lymphocytes is also severely depressed under low gravity conditions (Cogoli et al. 1984) because interleukin-2 (IL-2) and IL-2receptor gene expression are modified, the delivery of the costimulatory signal to activate the B7/CD28 pathway and the protein kinase A (PKA) signaling pathway, which is a key early regulator in T cell activation, are hindered. Furthermore, a TH2 cytokine shift is associated with spaceflight. If this TH2 shift persists during long missions, it could represent a significant clinical risk for TH2-related autoimmune diseases, allergies, hypersensitivities, and disease susceptibility related to diminished cell-mediated immunity. Studies on plasma antibody levels did not reveal significant changes after short spaceflights (Rykova et al. 2008), but contradictory results were reported after long missions. Indeed, several studies (Konstantinova et al. 1993; Bascove et al. 2008, 2009; Guéguinou et al. 2009, 2010) reported increased levels of immunoglobulin while Rykova et al. (2008) reported normal amounts of antibodies after prolonged space missions. Lastly, a differential sensitivity of cellular and humoral immunity to spaceflight conditions seems to exist because it was shown that the cellular, but not the humoral, systems are affected by short periods of flight. © 2012 Springer-Verlag Berlin Heidelberg. All rights are reserved.