Cytokine and adrenal axis responses to endotoxin

Low doses of lipopolysaccharide, tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), or exposure to a stressor (restraint) increased plasma corticosterone levels. In animals pretreated with lipopolysaccharide, a marked sensitization of the corticosterone response was evident upon subsequent exposure to lipopolysaccharide, TNF-alpha, or restraint, 1 day later. As well, the sickness-inducing effects of lipopolysaccharide, TNF-alpha and IL-1 beta were markedly increased in mice pretreated with lipopolysaccharide. The sensitization effects were marked when the second treatment was administered 1 day after lipopolysaccharide administration, but not when a 28-day interval elapsed. In a second experiment, TNF-alpha influenced monoamine functioning in the paraventricular nucleus of the hypothalamus and within extrahypothalamic regions, including the central amygdala, locus coeruleus, prefrontal cortex. Moreover, serotonin activity within the central amygdala, as well as dopamine activity within the prefrontal cortex, were subject to a sensitization effect in animals pretreated with lipopolysaccharide 1 day earlier. Macrophage depletion by a suspension of clodronate liposomes attenuated the plasma corticosterone changes induced by TNF-alpha, but did not affect the sensitization. In contrast, the acute effects of TNF-alpha on central neurotransmitters were unaffected by the liposome suspension, but this treatment prevented the sensitization. These data may be relevant to clinical situations in which individuals exposed to bacterial infections may be rendered more susceptible to the behavioural and neurochemical effects of subsequently encountered stressors and immunological challenges.

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“…The i.v. administration of the endotoxin increased hypothalamic IL‐1β levels (Ma et al ., 2000), both i.c.v. and i.v.…”

Section: Discussionmentioning

confidence: 99%

Central monoamine and plasma corticosterone changes induced by a bacterial endotoxin: sensitization and cross‐sensitization effects

Hayley

Lacosta

Merali

et al. 2001

Eur J of Neuroscience

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“…Lipopolysaccharide (LPS) potently suppresses food intake and increases the expression of inflammatory cytokines in numerous brain areas including the hypothalamus [21,22,23]. Administration of IL-1ra attenuates LPS-induced anorexia as well as LPS-induced hypothalamic expression of IL-1β, IL-6 and TNFα in mice [24].…”

Section: Inhibition Of Food Intake By Inflammatory Cytokines: Who Arementioning

confidence: 99%

Regulation of Food Intake by Inflammatory Cytokines in the Brain

Buchanan¹,

Johnson²

2007

Neuroendocrinology

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A number of inflammatory cytokines are synthesized and released after activation of the immune system. In addition to other biological effects, these cytokines can potently inhibit food intake. Cytokine-mediated inhibition of food intake is of particular importance because excessive production of peripheral inflammatory cytokines is often associated with the cachexia-anorexia syndrome seen in some chronic diseases. The weight loss in cachexia is associated with an increase in morbidity and mortality. Understanding how cytokines regulate food intake may be crucial in enhancing quality of life and facilitating recovery in patients exhibiting cachexia. This review describes the main inflammatory cytokines that influence food intake and explores how peripheral cytokines communicate with hypothalamic nuclei to influence feeding.

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“…IL-1 has an important role in the process of onset and continuation of inflammation [20]. IL-1 is a powerful effector of multiple connections among immune, nervous and endocrine systems [21].…”

Section: Serum Levels Of Il-1b In Different Conditionsmentioning

confidence: 99%

Involvement of Interleukin‐1β in Systemic Morphine Effects on Paw Oedema in a Mouse Model of Acute Inflammation

Pourpak

Ahmadiani²,

Alebouyeh³

2004

Scand J Immunol

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Recent studies suggest that peripheral morphine may represent a valuable treatment in acute inflammatory painful diseases through peripheral or central mechanisms. In the present study, anti-inflammatory effects of systemic morphine on carrageenan-induced hind paw oedema were examined in a model of peripheral acute oedema in mice. Carrageenan induced a time-dependent inflammation that was maximal 3 h after administration. While intraperitoneal administration of morphine sulfate at a low dose (1 mg/kg) increased carrageenan-induced hind paw oedema, intraperitoneal injection of morphine sulfate at a high dose (7 mg/kg) resulted in significant anti-inflammatory effects on carrageenan-induced hind paw oedema. These anti-inflammatory effects were blocked by pretreatment with naloxone. Measuring the serum levels of interleukin-1b revealed that increases in serum levels of this cytokine were involved in morphine anti-inflammatory effects. Pretreatment with naloxone decreased interleukin-1b serum levels near to those of control group. In conclusion, these data demonstrate that morphine produced pro-or anti-inflammatory effects in a dose-dependent manner through peripheral or central mechanisms. The observed anti-inflammatory effects may be due to an increase in the cytokine production and/or release by host immune systems.

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Cytokine and adrenal axis responses to endotoxin

Cited by 26 publications

References 37 publications

Central monoamine and plasma corticosterone changes induced by a bacterial endotoxin: sensitization and cross‐sensitization effects

Central monoamine and plasma corticosterone changes induced by a bacterial endotoxin: sensitization and cross‐sensitization effects

Regulation of Food Intake by Inflammatory Cytokines in the Brain

Involvement of Interleukin‐1β in Systemic Morphine Effects on Paw Oedema in a Mouse Model of Acute Inflammation

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