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Stress-induced Sympathetic Nervous System Activation Contributes to Both Suppressed Acquired Immunity and Potentiated Innate Immunity: The Role of Splenic NE Depletion and Extracellular Hsp72

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Neural and Neuroendocrine Mechanisms in Host Defense and Autoimmunity

Abstract

The following chapter will review the evidence that exposure to the same intense acute stressor can produce dichotomous effects on immune function and host defense that are dependent on the type of immune response tested and will develop the hypothesis that a common neuroendocrine mechanism exists for both outcomes, that is, activation of the sympathetic nervous system (SNS). First, I will describe research supporting the hypothesis that excessive SNS activation can produce suppression of a measure of acquired immunity, the in vivo antibody response to a benign protein. Importantly, only “excessive” SNS activation can produce the immunosuppression. Frequently, stressor exposure stimulates the SNS response but does not excessively drive the response to produce a state of catecholamine depletion in innervated tissues.We predict in the absence of tissue norepinephrine (NE) depletion, stimulation of the SNS will not suppress acquired immunity. Second, I will review the research supporting the hypothesis that stress-induced activation of SNS facilitates innate immune host defense. The role of the SNS in stress-induced potentiation of innate immunity contrasts with that of SNS effects on acquired immunity in that it does not depend on excessive SNS drive or tissue catecholamine depletion. In our studies, innate immune function was assessed by measuring the host’s initial response to an in vivo bacterial challenge that depends on innate and not acquired immune cells (Campisi et al., 2005).

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Fleshner, M. (2006). Stress-induced Sympathetic Nervous System Activation Contributes to Both Suppressed Acquired Immunity and Potentiated Innate Immunity: The Role of Splenic NE Depletion and Extracellular Hsp72. In: Welsh, C.J., Meagher, M.W., Sternberg, E.M. (eds) Neural and Neuroendocrine Mechanisms in Host Defense and Autoimmunity. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-48334-4_3

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