Cytokines, PGE2 and endotoxic fever: a re-assessment

Blatteis, Clark M.; Li, Shuxin; Li, Zhonghua; Feleder, Carlos; Perlik, Vit

doi:10.1016/j.prostaglandins.2005.01.001

Cited by 145 publications

(111 citation statements)

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“…It is believed that fever genesis begins with the production of pyrogenic cytokines by mononuclear cells, their release into the peripheral blood stream and transport to the hypothalamus, and their production of PGE 2 (10,11). The present results further demonstrated that the increased levels of PGE 2 in the hypothalamus induced by LPS could be suppressed by aspirin pretreatment.…”

Section: Discussionsupporting

confidence: 73%

“…of LPS caused a monophasic fever, while larger doses (2 -10 µg / kg) of LPS caused a biphasic fever. Evidence has accumulated to suggest that the steps that lead to fever genesis is that they start with the production of pyrogenic cytokines by mononuclear cells, their release into the peripheral blood stream and transport to the hypothalamus, and their formation of cyclooxygenase-2 (COX-2)-dependent PGE 2 (11). It postulates that the early phase of the LPS-induced fever denotes an antioxidant-sensitive PGE 2 rise, while the late phase of the LPS-induced fever represents a delayed PGE 2 -dependent Tco rise.…”

Section: Discussionmentioning

confidence: 99%

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Aspirin May Exert Its Antipyresis by Inhibiting the N-Methyl-D-aspartate Receptor-Dependent Hydroxyl Radical Pathways in the Hypothalamus

et al. 2007

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Abstract. Recent findings have suggested that the N-methyl-D-aspartate (NMDA) receptordependent hydroxyl radical pathway in the hypothalamus of rabbit brain may mediate the fever induced by lipopolysaccharide (LPS). The aim of this study was to investigate whether aspirin exerts its antipyresis by suppressing hypothalamic glutamate and hydroxyl radicals in rabbits. The microdialysis probes were stereotaxically and chronically implanted into the preoptic anterior hypothalamus of rabbit brain for determination of both glutamate and hydroxyl radicals in situ. It was found that intravenous (i.v.) injection of LPS, in addition to inducing fever, caused increased levels of both glutamate and hydroxyl radicals in the hypothalamus. Pretreatment with aspirin (10 -60 mg / kg, i.v.) one hour before an i.v. dose of LPS significantly reduced the febrile response and attenuated the LPS-induced increased levels of both glutamate and hydroxyl radicals in the hypothalamus. The increased levels of prostaglandin E 2 (PGE 2 ) in the hypothalamus induced by LPS could be suppressed by aspirin pretreatment. The data indicate that systemic administration of aspirin, in addition to suppressing PGE 2 production, may exert its antipyresis by inhibiting the NMDA receptor-dependent hydroxyl radical pathways in the hypothalamus during LPS fever.

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Aspirin May Exert Its Antipyresis by Inhibiting the N-Methyl-D-aspartate Receptor-Dependent Hydroxyl Radical Pathways in the Hypothalamus

et al. 2007

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“…Rats given LPS as adults show well-documented increases in circulating levels of the proinflammatory cytokines TNF-␣ and IL-6 (8,17,19). We have previously demonstrated significant reductions in the levels of the LPS-stimulated proinflammatory cytokines in LPS-treated adults given LPS at P14 (17).…”

Section: Discussionmentioning

confidence: 91%

Neonatal immune challenge does not affect body weight regulation in rats

Spencer¹,

Mouihate²,

Galic³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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The perinatal environment plays a crucial role in programming many aspects of adult physiology. Myriad stressors during pregnancy, from maternal immune challenge to nutritional deficiency, can alter longterm body weight set points of the offspring. In light of the increasing concern over body weight issues, such as obesity and anorexia, in modern societies and accumulating evidence that developmental stressors have long-lasting effects on other aspects of physiology (e.g., fever, pain), we explored the role of immune system activation during neonatal development and its impact on body weight regulation in adulthood. Here we present a thorough evaluation of the effects of immune system activation (LPS, 100 g/kg ip) at postnatal days 3, 7, or 14 on long-term body weight, adiposity, and body weight regulation after a further LPS injection (50 g/kg ip) or fasting and basal and LPS-induced circulating levels of the appetite-regulating proinflammatory cytokine leptin. We show that neonatal exposure to LPS at various times during the neonatal period has no long-term effects on growth, body weight, or adiposity. We also observed no effects on body weight regulation in response to a short fasting period or a further exposure to LPS. Despite reductions in circulating leptin levels in response to LPS during the neonatal period, no long-term effects on leptin were seen. These results convincingly demonstrate that adult body weight and weight regulation are, unlike many other aspects of adult physiology, resistant to programming by a febrile-dose neonatal immune challenge.gender; leptin; lipopolysaccharide; obesity THE PERINATAL ENVIRONMENT is known to play a crucial role in programming body weight. In humans, low birth weight and malnutrition during gestation have been linked with abdominal obesity in adulthood (31,45,46). Similarly, a variety of behavioral, physiological (including dietary manipulations), and immune stressors given to pregnant experimental animals have been reported to alter the body weight of adult offspring (4,15,27,36,40,63). It appears, however, that the timing of perinatal stress is critical in programming many aspects of adult physiology (35) and relatively little is known regarding the influence of postnatal stress on adult body weight regulation.The long-term physiological consequences of a neonatal immune challenge with LPS have been extensively described by our laboratory and others. For example, we have shown attenuated febrile and associated host defense responses in adulthood to an immune challenge of the same type as that experienced at postnatal day (P) 14 (9,17,18). Changes have also been demonstrated in memory processing (7), hypothalamic-pituitary-adrenal axis activation (51, 52), and susceptibility to pathological insults in adulthood (10, 55, 56). However, the long-term effects of a neonatal immune challenge on body weight regulation are less clear, and given the concern over the current obesity epidemic in modern society [e.g., (29)], demand further investigation. For instance, Walker ...

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“…The role of PGE 2 in induction of fever in mammals was already reported in 1971 by Milton and Wendlandt (1971) who demonstrated that microinjection of PGE 2 into the third ventricle of conscious cats and rabbits cause a rise of body temperature. The subsequent studies using inhibitors of PGE 2 synthesis clearly confirmed that PGE 2 plays essential role in fever expressed by mammals (reviewed by Ivanov and Romanovsky, 2004;Blatteis et al, 2005). PGE 2 biosynthesis involves three successive enzymatic reactions (Pecchi et al, 2009): firstly, arachidonic acid (AA) is released by the action of phospholipase A2 (PLA2) on the cell membrane phospholipids; secondly, AA is metabolized in PGG 2 then converted to PGH 2 by the action of COX; thirdly, PGH 2 is finally metabolized in PGE 2 by the mPGES1.…”

Section: The Key Role Of Pgementioning

confidence: 85%

Behavioral fever in ectothermic vertebrates

Rakus

Ronsmans

Vanderplasschen

2017

Developmental & Comparative Immunology

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a b s t r a c tFever is an evolutionary conserved defense mechanism which is present in both endothermic and ectothermic vertebrates. Ectotherms in response to infection can increase their body temperature by moving to warmer places. This process is known as behavioral fever. In this review, we summarize the current knowledge on the mechanisms of induction of fever in mammals. We further discuss the evolutionary conserved mechanisms existing between fever of mammals and behavioral fever of ectothermic vertebrates. Finally, the experimental evidences supporting an adaptive value of behavioral fever expressed by ectothermic vertebrates are summarized.

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Cytokines, PGE2 and endotoxic fever: a re-assessment

Cited by 145 publications

References 100 publications

Aspirin May Exert Its Antipyresis by Inhibiting the N-Methyl-D-aspartate Receptor-Dependent Hydroxyl Radical Pathways in the Hypothalamus

Aspirin May Exert Its Antipyresis by Inhibiting the N-Methyl-D-aspartate Receptor-Dependent Hydroxyl Radical Pathways in the Hypothalamus

Neonatal immune challenge does not affect body weight regulation in rats

Behavioral fever in ectothermic vertebrates

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