151. Effects of breast cancer risk and psychological distress on immune responses in healthy women

151. Effects of breast cancer risk and psychological distress on immune responses in healthy women

Abstracts / Brain, Behavior, and Immunity 22 (2008) 43–49 151. Effects of breast cancer risk and psychological distress on immune responses in healthy...

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Abstracts / Brain, Behavior, and Immunity 22 (2008) 43–49 151. Effects of breast cancer risk and psychological distress on immune responses in healthy women Na-Jin Park *, Duck-Hee Kang School of Nursing, University of Alabama at Birmingham, Birmingham, AL 35226, USA * Corresponding author. E-mail: [email protected]

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152. Sleep, sleep deprivation and responses to lipopolysaccharide of interleukin-1b receptor 1 and tumor necrosis factor-a receptor 1 double knockout mice Francesca Baracchi a,*, Mark Opp a,b,c a Department of Anesthesiology University of Michigan, Ann Arbor, MI, USA b Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI, USA c Neuroscience Graduate Program, University of Michigan, Ann Arbor, MI, USA * Corresponding author. E-mail: [email protected]

Breast cancer (BC) risk, whether assessed objectively or subjectively, may influence immune responses such as natural killer cell activity (NKCA) in healthy women. High subjective risk may lead to high psychological distress, which may, in turn, negatively affect immune responses. However, these potential influences are unknown, as research has been limited in this area. Objectives of the study were to examine: (1) the main effects of objective and subjective BC risk on NKCA; and (2) the mediating role of psychological distress in the relationship between subjective BC risk and NKCA in healthy women at varying levels of BC risk. For this cross-sectional study, 117 healthy women (mean age 36.5 years) completed questionnaires and gave a blood sample for NKCA measurements. Objective BC risk was calculated based on the modified Gail model. Regression analyses revealed a significant inverse association between objective risk and NKCA at the 12.5:1 effector-to-target ratio (p = .013), whereas subjective risk showed no effect on NKCA after controlling for current birth control pill use. Current birth control pill users had significantly lower NKCA at all four ratios than non users. Because of the lack of main effect of subjective BC risk on NKCA, the mediating role of psychological distress was not tested. There was, however, a direct association between subjective BC risk and psychological distress. Objective and subjective BC risks have different contributions to psycho-immune profiles in healthy women. Given the importance of NKCA in early tumor defense, the impact of objective BC risk on NKCA needs to be further investigated.

IL-1b and TNFa are well characterized sleep regulatory substances. We used mice lacking both the IL-1b receptor 1 and TNF±; receptor 1 (double KO) to further investigate roles for IL-1b and TNF±; in sleep regulation and in responses to immune challenge. Male double KO and B6129SFs/J control mice were surgically implanted with EEG electrodes and a thermistor to record brain temperature. After recovery, 48 h undisturbed baseline recordings were obtained. Mice were then sleep deprived for 6 h at the beginning of the light period. After several days, mice were injected intraperitoneally with vehicle and on a subsequent day with LPS. Double KO mice spent less time in non-rapid eye movement sleep (NREMS) during the dark period and less time in rapid eye movement sleep (REMS) during the light period. After sleep deprivation, control mice exhibited prolonged increases in NREMS and REMS, whereas in double KO mice the duration of the NREMS increase was shorter and there was no increase in REMS. The LPS-induced increase in NREMS of double KO mice was less than that of control mice. LPS suppressed REMS of control mice for 12 h, and of the double KO mice for 6 h. These data demonstrate that the lack of both IL-1R1 and TNFR1 alters baseline sleep, impairs compensatory responses to sleep deprivation, and reduces the effects of LPS on sleep-wake behavior when administered prior to light onset. These results further implicate IL-1 and TNF in the regulation of physiological sleep and in the alterations in sleep that occur after immune challenge.

doi:10.1016/j.bbi.2008.04.153

doi:10.1016/j.bbi.2008.04.154