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SPACEFLIGHT AND IMMUNITY IN THE MOUSE: PART I. M.J. Pecaut¹, G.A. Nelson¹, L.L. Peters⁵, P.J. Kostenuik⁶, T.A. Bateman^3,4, S. Moroney⁶, L.S. Stodiek³, D.L. Lacey⁶, S.J. Simske³, and D.S. Gridley^1,2. Depts of ¹Radiation Medicine and ²Biochemistry & Microbiology, Loma Linda Univ. & Medical Center, Loma Linda, CA; ³Dept of Aerospace Engineering, BioServe Space Technologies, Univ of Colorado, Boulder, CO; ⁴Biomedical Engineering Program, Mech Engineering Dept, Colorado State Univ, Fort Collins, CO; ⁵The Jackson Laboratory, Bar Harbor, ME; & ⁶Amgen Inc., Thousand Oaks, CA.

  On December 5^th, 2001, the Space Shuttle Endeavor (STS-108/UF-1) launched for a 12-day mission to examine the effects of spaceflight on physiology in the C57BL/6 mouse model. Mission-related psychological stress, low-dose/low-dose-rate radiation, and changes in inertial condition have all already been shown to influence immunity in humans and rat models. However, this is the first time the mouse model has been utilized to examine these systems.  Within 3-5 hours of their return, the mice were euthanized and dissected. Immunological assays were performed on the spleen, blood, and bone marrow. Exposure to spaceflight did not significantly alter general circulating leukocyte percentages. However, splenic lymphocyte percentages increased while granulocyte percentages decreased. Flow cytometric analysis of splenic lymphocytes indicated there was a shift away from CD3+ T cells toward B220+ B cells.  Decreases in splenic CD3+/CD4+ helper T cells resulted in an overall decrease in the CD4:CD8 ratio. In contrast, there were increases in bone marrow T cells, with decreases in B cells.  Additionally, although the total blast population decreased, CD34+ cells increased. As this is the first time these analyses have been conducted in a mouse model after spaceflight, there is little to which the results can be directly compared. However, many of the results are similar to those of past flights with rat models and humans. Rather than isolated peripheral changes, the shift in bone marrow populations is more consistent with a shift in hematopoiesis. Because there also appear to be shifts in populations involved in cellular and humoral immune defense mechanisms, responses to bacterial and/or viral pathogens may be less than optimal.

(Supported by NASA: Coop. Agreement NCC9-149)

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