Cold water stress and immunological responsiveness

Animal models can advance the knowledge of how neuroendocrine-mediated host stress responses modulate immune cell function. These animal models can be used to evaluate whether immunological perturbations following exposure to acute and chronic stressors are of clinical significance in resistance to infectious and neoplastic diseases. In the present study, we evaluated parameters of immunological structure and function in mice exposed to cold water stress. We exposed young adult male BDFl mice to 4°C water for 1 minute at 0900 and 1600 on each of 4 consecutive days. The treatment regimen invokes a complex paradigm of anxiety, forced exercise and hypothermia. Glucocorticoid production was enhanced on days 2 (P=0.011) and 3 (P=0.026). Exposure to the cold water stress regimen did not result in atrophy of or leukopenia in the spleen or thymus. Single fluorescence flow cytometric analysis revealed profiles of CD3, CD4, and CD8 populations in the spleen and thymus were not altered following exposure to the cold water stress treatment. Exposure to the stressor inhibited concanavalin A (ConA)-stimulated lymphocyte blastogenic potential in thymocytes (P=0.024) but not splenocytes (P>0.050). Profiles of IL-2 production (P=0.031; as measured by ELISA), but not IFN production (P>0.050; as measured by bioassay) were altered by exposure to the cold water stressor. Exposure to the stressor did not inhibit profiles of immune responses to the immunogen cholera toxin binding fragment (CTB), as revealed by splenocyte proliferation, IL-2 and EFN production, and titers of anti-CTB antibody. Collectively, these results indicate that exposure to acute periods of cold water stress can result in mild immunomodulatory effects in mice which are not sufficient to impair response to the protein antigen CTB.