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Thermal Stress and Immunity

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Thermotherapy for Neoplasia, Inflammation, and Pain

Summary

The rise in deep-body temperature is etiologically categorized into active hyperthermia and passive hyperthermia. A typical example of active hyperthermia is fever. Fever is a centrally regulated rise in core ternperature that is primarily determined by changes in the activity of hypothalamic thermosensitive neurons in response to both pyrogenic cytokines and cryogenic substances derived from the biodefense system. Fever is a phylogenetically old phenomenon observed in invertebrates as well as in vertebrates. Although fever is occasionally harmful, it is likely that fever has evolved as an adaptive host defense response to infection. The febrile temperature exerts detrimental effects on the growth of microorganisms and enhancing effects on T-cellmediated immunity in vitro. Although some functions of the natural immunity (natural killer cell activity and the production of cytokines by macrophages) are suppressed at febrile temperatures, it is presumed that the net effect of febrile temperature on both attacking factors and host defense activities may promote the survival rate of the infected host. Passive hyperthermia as a result of inadequate heat loss in a warm environment, if it is severe, enhances bacterial translocation across the gut mucosal barrier. The gut-derived endotoxin triggers the production of pyrogenic cytokines in the mesenteric lymphoid tissues and liver. Thus, such cytokines activate the immune system on one hand and potentially aggravate environmentally or behaviorally (e.g., exercise) induced hyperthermia by their pyrogenic actions.

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Authors and Affiliations

  1. Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan

    Tetsuro Hori, Yasuo Kaizuka, Atsushi Takaki & Toshihiko Katafuchi

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  1. Tetsuro Hori
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  2. Yasuo Kaizuka
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  3. Atsushi Takaki
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  4. Toshihiko Katafuchi
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Editors and Affiliations

  1. Department of Environmental Physiology, Institute of Tropical Medicine, Nagasaki University, 852-8523, Nagasaki, Japan

    Mitsuo Kosaka

  2. Health Research Foundation, 606-8225, Kyoto, Japan

    Tsutomu Sugahara

  3. Clinic of Rheumatology, Physical Medicine, and Balneology, University of Giessen, Bad Nauheim, Germany

    Klaus L. Schmidt

  4. Max Planck Institute for Physiological and Clinical Research, W.G. Kerckhoff Institute, Bad Nauheim, Germany

    Eckhart Simon

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Hori, T., Kaizuka, Y., Takaki, A., Katafuchi, T. (2001). Thermal Stress and Immunity. In: Kosaka, M., Sugahara, T., Schmidt, K.L., Simon, E. (eds) Thermotherapy for Neoplasia, Inflammation, and Pain. Springer, Tokyo. https://doi.org/10.1007/978-4-431-67035-3_27

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  • DOI: https://doi.org/10.1007/978-4-431-67035-3_27

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