Stress-induced hyperthermia and infection-induced fever: Two of a kind?

Vinkers, Christiaan H.; Groenink, Lucianne; Bogaert, Meg J.V. van; Westphal, Koen G.C.; Kalkman, Cor J.; Oorschot, Ruud van; Oosting, Ronald S.; Olivier, Berend; Korte, S. Mechiel

doi:10.1016/j.physbeh.2009.04.004

Cited by 69 publications

(73 citation statements)

References 54 publications

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“…For example, stress-induced hyperthermia, but not infection-induced fever, is attenuated by anxiolytic drugs, such as diazepam (Fig. 8B) (76,122,178,193), whereas cyclooxygenase inhibitors block infection-induced fever, but not stress-induced hyperthermia (76,155,178,182,188). Furthermore, EP3 receptor-deficient mice can exhibit intact stressinduced hyperthermia, but fail to exhibit LPS-induced fever (119).…”

Section: Psychological Stress-induced Hyperthermiamentioning

confidence: 99%

Central circuitries for body temperature regulation and fever

Nakamura

2011

American Journal of Physiology-Regulatory, Integrative and Comp

432

394

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Nakamura K. Central circuitries for body temperature regulation and fever. Am J Physiol Regul Integr Comp Physiol 301: R1207-R1228, 2011. First published September 7, 2011 doi:10.1152/ajpregu.00109.2011.-Body temperature regulation is a fundamental homeostatic function that is governed by the central nervous system in homeothermic animals, including humans. The central thermoregulatory system also functions for host defense from invading pathogens by elevating body core temperature, a response known as fever. Thermoregulation and fever involve a variety of involuntary effector responses, and this review summarizes the current understandings of the central circuitry mechanisms that underlie nonshivering thermogenesis in brown adipose tissue, shivering thermogenesis in skeletal muscles, thermoregulatory cardiac regulation, heat-loss regulation through cutaneous vasomotion, and ACTH release. To defend thermal homeostasis from environmental thermal challenges, feedforward thermosensory information on environmental temperature sensed by skin thermoreceptors ascends through the spinal cord and lateral parabrachial nucleus to the preoptic area (POA). The POA also receives feedback signals from local thermosensitive neurons, as well as pyrogenic signals of prostaglandin E 2 produced in response to infection. These afferent signals are integrated and affect the activity of GABAergic inhibitory projection neurons descending from the POA to the dorsomedial hypothalamus (DMH) or to the rostral medullary raphe region (rMR). Attenuation of the descending inhibition by cooling or pyrogenic signals leads to disinhibition of thermogenic neurons in the DMH and sympathetic and somatic premotor neurons in the rMR, which then drive spinal motor output mechanisms to elicit thermogenesis, tachycardia, and cutaneous vasoconstriction. Warming signals enhance the descending inhibition from the POA to inhibit the motor outputs, resulting in cutaneous vasodilation and inhibited thermogenesis. This central thermoregulatory mechanism also functions for metabolic regulation and stress-induced hyperthermia.

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Section: Psychological Stress-induced Hyperthermiamentioning

confidence: 99%

Central circuitries for body temperature regulation and fever

Nakamura

2011

American Journal of Physiology-Regulatory, Integrative and Comp

432

394

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“…Research shows that artificially synthesise interleukins had been used in treatment of the following; post surgery in patient with chronic hepatitis B infection [21], in HIV infection [22], in cancer treatment [23]. Findings also shows the relation of fever and immune response [24] and hyperthermia [25] physioanatobiochemical processes [26].…”

Section: Physioanatomical Roles Of the Immune System Entities In Longmentioning

confidence: 99%

A Novel Automated Immune Boosting Machine (Blueprint Glimpse) Which May Increase Life Span and Insight into Unexploited Benefits of Febrile Responses (Fever)

Sani¹

2015

J Med Diagn Meth

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Definition of new termsSpecial treatment room is a specially designed room in the hospital where the machine will be house. VBBI is values of strength of the immune systems following exposure to the machine, ISI is the immune strength time span. IP is immune power actual ability of immune system to fight off or attenuate an attack. AbstractThe essence of the review is to demonstrate the following, the evolution of a novel machine that could boost the body immune system, treat through hyperthermia, existing body abnormalities linked with febrilar response, and make formidable the immune system if routine weekly exposure of individuals, whether or not in ill health is done, and again the operation of the machine will focus on adjustment of bio-thermal circles pertinent to induced pyrogen (for routine treatment) and non-induce non-pyrogen (as found in ill health) such that immediate immune response effectively, could combat existing disease in addition to protecting the body against futures attacks generally. Febrile responses mediators, broadly speaking encompass dual types, pyrogens and non-pyrogen, pyrogens mediated are inducible even in absence of disease or abnormal condition, non pyrogen febrilar reponses usually emanate from disease or abnormal condition of the body (cancer, infectious disease and non infectious disease) in either case, resultant hypethermia and immune responses are secondary to altered cellular physiological processes, among them are increases or decrease in metabolism of fuels molecules of the cells, mobilisation of mineral elements iron for instance, acute phase protein mobilisation, increase in uptake of de novo synthesize survival materials (may increase life span), activations of immune system chain reaction by secretion of immunological communicants such as cytokines and chemokines, sensitization and recruitment of other immune cells, ultimately also includes interactions between autocoids and some immunes cells, and as determined by the hypothalamic thermostat leading to increase in body defence mechanism and well being. Erroneously, temperature increase is seen as fever, however on the contrary, hyperthermal events is just one among many of it manifestations, for actually fever is systemic attempts to fight off pathological or abnormal attacks in the internal milieu, past finding adduced that fever is associated with many disease or abnormality, a fact that depict a need for further research on survival value of fever, it has survival value (Kluger 1998), results obtained using mathematical methods in a novel way from previous finding results and standard reference physioantobiochemical values were analysed with SPSS analytical package, dependent variables (Immune Strength Index (ISI), Values of Boosted Body Immunity (VBBI), PARPS, Survival values, Life span increase) and independent variables (incremental values of febrile temperature values of pyrogen used, number of exposure to the machine) show strong correlation P ≤ 0.005, temperature and survival value (increase in life span)...

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“…On the other hand, a variety of acute or short-term stresses including psychological stress increase body temperature in rats [6,7], mice [8,9,10,] and humans [11,12,13,14,15]. The acute stress-induced hyperthermia and infection-induced fever are considered to be 2 distinct processes mediated largely by different neurobiological mechanisms [7], although they result in similar clinical signs, that is, higher body temperature accompanied by shivering and cutaneous vasoconstriction [16]. Nonetheless, the influence of chronic or long-term stress on thermoregulation still remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Enhanced Hyperthermic Responses to Lipopolysaccharide in Mice Exposed to Repeated Cold Stress

Miyamoto

Funakami²,

Kawashita³

et al. 2017

Pharmacology

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Lipopolysaccharide (LPS) induces hyperthermia accompanied by various other systemic inflammatory symptoms. The rodents exposed to repeated cold (RC) stress according to a specific schedule are useful as experimental models for autonomic imbalance or fibromyalgia. It is now proven that RC-stressed mice exhibit tolerance to LPS, we examined thermal responses to LPS challenge in RC-stressed mice by monitoring core temperature using the telemetry system. Systemic administration of LPS caused bimodal hyperthermic responses in RC-stressed and unstressed mice. The magnitude of the LPS-induced hyperthermia was greater in RC-stressed mice than in unstressed mice. The RC stress-induced enhancement of hyperthermic responses to LPS was abolished by pretreatment with diclofenac, which is a cyclooxygenase (COX) inhibitor. LPS did not significantly increase COX-2 protein levels in the lung or hypothalamus of RC-stressed or unstressed mice. RC stress did not alter baseline serum corticosterone levels or their increases in response to LPS challenge. These results suggest that RC stress enhances the susceptibility of mice to LPS challenge, leading to greater prostanoid-dependent hyperthermia, which might contribute to tolerance to LPS in RC-stressed mice.

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Stress-induced hyperthermia and infection-induced fever: Two of a kind?

Cited by 69 publications

References 54 publications

Central circuitries for body temperature regulation and fever

Central circuitries for body temperature regulation and fever

A Novel Automated Immune Boosting Machine (Blueprint Glimpse) Which May Increase Life Span and Insight into Unexploited Benefits of Febrile Responses (Fever)

Enhanced Hyperthermic Responses to Lipopolysaccharide in Mice Exposed to Repeated Cold Stress

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