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      Effects of Sexual Arousal on Lymphocyte Subset Circulation and Cytokine Production in Man

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          Abstract

          Objective: Sexual arousal and orgasm induce an increase in sympathetic activity as well as in catecholamine and prolactin plasma concentrations. However, the effects of sexual arousal and orgasm on immune functions in man are unknown. Thus, this study investigated the effects of masturbation-induced orgasm on lymphocyte circulation and cytokine production in healthy young males. Methods: In a crossover design, 11 volunteers completed an experimental condition in which they were asked to masturbate until orgasm and to participate in a control condition without sexual activity. Blood was drawn continuously for determination of endocrine parameters. In addition, leukocyte and lymphocyte subsets were analyzed via flow cytometry, and the production of lipopolysaccharide-induced interleukin 6 and tumor necrosis factor alpha was measured before and then 5 and 45 min after the orgasm. Results: The results confirmed transient increases in adrenaline and prolactin plasma concentrations. Sexual arousal and orgasm increased the absolute number of leukocytes, in particular natural killer cells (CD3–CD16+CD56+), in the peripheral blood. In contrast, T cell (CD3+) and B cell (CD3–CD20+) subpopulations as well as the production of interleukin 6 and tumor necrosins factor alpha remained unaffected by sexual activity. Conclusion: These findings demonstrate that components of the innate immune system are activated by sexual arousal and orgasm.

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          Most cited references15

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          The relationship of depression and stressors to immunological assays: a meta-analytic review.

          This is a broad meta-analysis of the relations of both depression and stressors to immunological assays. The number of study samples (greater than 180) and measures (greater than 40) is much more extensive than any so far. Analyses are done by both fixed and random effects. By a fixed-effects analysis, both major depression and naturally occurring acute stressors are associated with (1) an overall leukocytosis, (2) mild reductions in absolute NK-cell counts and relative T-cell proportions, (3) marginal increases in CD4/CD8 ratios, and (4) moderate decreases in T- and NK-cell function. However, the degree of heterogeneity of the studies' results raises questions about their robustness. Therefore, we also did the first random effects analysis to estimate what is likely to appear in future studies. For depression, the analysis showed the immunological correlates included (1) an overall leukocytosis, manifesting as a relative neutrophilia and lymphoenia; (2) increased CD4/CD8 ratios; (3) increased circulating haptoglobin, PGE(2), and IL-6 levels; (4) reduced NK-cell cytotoxicity; and (5) reduced lymphocyte proliferative response to mitogen. For stressors, the random effects analysis showed that future studies are likely to find the following effects: (1) an overall leukocytosis, manifesting as an absolute lymphocytosis; (2) alterations in cytotoxic lymphocyte levels, CD4/CD8 ratios, and natural killer cell cytotoxicity with the direction of change depending on the chronicity of the stressor; (3) a relative reduction of T-cell levels; (3) increased EBV antibody titers; (4) reduced lymphocyte proliferative response and proportion of IL-2r bearing cells following mitogenic stimulation; and (5) increased leukocyte adhesiveness. The random-effects analysis revealed that for both major depression and naturally occurring stressors the following effects are shared: leukocytosis, increased CD4/CD8 ratios, reduced proliferative response to mitogen, and reduced NK cell cytotoxicity. The implications for these findings for disease susceptibility and the pathophysiology of these conditions is discussed. Copyright 2001 Academic Press.
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            Increased sexual activity reduces male immune function in Drosophila melanogaster.

            Despite the benefits of resistance, susceptibility to infectious disease is commonplace. Although specific susceptibility may be considered an inevitable consequence of the co-evolutionary arms race between parasite and host, a more general constraint may arise from the cost of an immune response. This "cost" hypothesis predicts a tradeoff between immune defense and other components of fitness. In particular, a tradeoff between immunity and sexually selected male behavior has been proposed. Here we provide experimental support for the direct phenotypic tradeoff between sexual activity and immunity by studying the antibacterial immune response in Drosophila melanogaster. Males exposed to more females showed a reduced ability to clear a bacterial infection, an effect that we experimentally link to changes in sexual activity. Our results suggest immunosuppression is an important cost of reproduction and that immune function and levels of disease susceptibility will be influenced by sexual selection.
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              Promiscuity and the primate immune system.

              The behavioral and ecological factors involved in immune system evolution remain poorly explored. We present a phylogenetic analysis of white blood cell counts in primates to test three hypotheses related to disease risk: increases in risk are expected with group size or population density, exposure to soil-borne pathogens, and mating promiscuity. White blood cell counts were significantly greater in species where females have more mating partners, indicating that the risk of sexually transmitted disease is likely to be a major factor leading to systematic differences in the primate immune system.
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                Author and article information

                Journal
                Neuroimmunomodulation
                Neuroimmunomodulation
                S. Karger AG
                1021-7401
                1423-0216
                August 1 2004
                August 20 2004
                : 11
                : 5
                : 293-298
                Article
                10.1159/000079409
                71cbb2b2-5307-40f3-831b-292d366660a0
                © 2004

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