Expression of interleukin 1α, interleukin 1β and interleukin 1 receptor antagonist mRNA in mouse brain: regulation by bacterial lipopolysaccharide (LPS) treatment

Gabellec, Marie-Madeleine; Griffais, Rémi; Fillion, G.

doi:10.1016/0169-328x(95)00042-q

Cited by 140 publications

(64 citation statements)

References 48 publications

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“…In line with the current study, there are several other reports of a modest elevation of non-stimulated IL-6 levels within the aging brain [19,53]. There is previously published evidence that systemically administered LPS is able to rapidly and directly target the CNS [21,15,22,49].…”

Section: Discussionsupporting

confidence: 92%

Dietary melatonin selectively reverses age-related changes in cortical cytokine mRNA levels, and their responses to an inflammatory stimulus

Sharman

Yang

et al. 2002

Neurobiology of Aging

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The basal levels of expression of mRNA of cytokines, interleukin-6 (IL-6) and tumor necrosis factor (TNF-␣), in the cerebral cortex of 5 and 26 month-old male B6C3F1 mice have been compared. In addition, the responsivity of animals of differing age to an inflammatory stimulus (lipopolysaccharide, LPS) has been studied. Basal levels of both of these cytokine mRNAs were elevated in aged animals relative to the younger group. However LPS administration led to a robust increase in cytokine mRNA levels in the younger animals but in aged mice, there was either an unchanged (IL-6) or a depressed (TNF-␣) response. Administration of dietary melatonin (200 ppm) to aged mice for 6 weeks prior to sacrifice, resulted in reduction of basal levels of cytokine mRNA to values found in the younger animals. Furthermore, following administration of LPS to melatonin fed animals, cerebral cytokine mRNA levels were significantly elevated rather than being unchanged or depressed. Taken together these findings reflect a trend in the cortices of melatonin-treated aged mice, to more closely approximate the status of younger mice. For comparative purposes, parallel studies were carried out using an immunologically active organ (spleen) and a non-neural organ with a low rate of cell turnover (heart muscle). In both these tissues, basal levels of cytokine mRNAs of animals of either age were very low, and there was a marked positive response to LPS. Dietary melatonin had no effect on the responses of TNF-␣ mRNA to LPS but attenuated the reaction of splenic IL-6 mRNA, thus bringing the response closer to that of the younger mice.

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Section: Discussionsupporting

confidence: 92%

Dietary melatonin selectively reverses age-related changes in cortical cytokine mRNA levels, and their responses to an inflammatory stimulus

Sharman

Yang

et al. 2002

Neurobiology of Aging

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“…In response to the peripheral administration of LPS, the CNS expresses elevated levels of TNF-␣ mRNA (Gatti and Bartfai, 1993;Breder et al, 1994;Laye et al, 1994;Liu et al, 1996;Pitossi et al, 1997), as well as other inflammation-related cytokines such as IL-1 and IL-6 (Ban et al, 1992;van Dam et al, 1992van Dam et al, , 1995Gatti and Bartfai, 1993;Muramami et al, 1993;Laye et al, 1994Laye et al, , 1995Quan et al, 1994;Buttini and Boddeke, 1995;Gabellec et al, 1995;Pitossi et al, 1997). Thus it has been proposed that the changes in CNS function (e.g., fever, sickness, behavior, activation of the HPA axis) during endotoxemia may be attributable to the influence of cytokines generated within the CNS (Kakucska et al, 1993;Klir et al, 1993;Roth et al, 1993;Hopkins and Rothwell, 1995;Laye et al, 1995;Rothwell and Hopkins, 1995).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Tumor Necrosis Factor-α Action within the CNS Markedly Reduces the Plasma Adrenocorticotropin Response to Peripheral Local Inflammation in Rats

et al. 1997

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The present study tested the hypothesis that the cytokine tumor necrosis factor-α (TNF-α) is an important CNS mediator of the hypothalamo-pituitary-adrenal (HPA) axis response to local inflammation in the rat. Recombinant murine TNF-α administered directly into the cerebroventricles of normal rats produced a dose-dependent increase in plasma adrenocorticotropin (ACTH) concentration. Local inflammation induced by the intramuscular injection of turpentine (50 μl/100 gm body weight) also produced an increase in plasma ACTH, peaking at 160–200 pg/ml at 7.5 hr after injection (compared with 10–30 pg/ml in controls). Intracerebroventricular pretreatment with either 5 μl of anti-TNF-α antiserum or 1–50 μg of soluble TNF receptor construct (rhTNFR:Fc) reduced the peak of the ACTH response to local inflammation by 62–72%. In contrast, intravenous treatment with the same doses of anti-TNF-α or rhTNFR:Fc had no significant effect on the ACTH response to local inflammation. Although these data indicated an action of TNF-α specifically within the brain, no increase in brain TNF-α protein (measured by bioassay) or mRNA (assessed using eitherin situhybridization histochemical or semi-quantitative RT-PCR procedures) was demonstrable during the onset or peak of HPA activation produced by local inflammation. Furthermore, increased passage of TNF-α from blood to brain seems unlikely, because inflammation did not affect plasma TNF-α biological activity. Collectively these data demonstrate that TNF-α action within the brain is critical to the elaboration of the HPA axis response to local inflammation in the rat, but they indicate that increases in cerebral TNF-α synthesis are not a necessary accompaniment.

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“…Neurons in various brain areas increase expression of several pro-inflammatory cytokines, their accessory proteins and their receptors in response to peripheral administration of LPS (Gabellec et al 1995;Gayle et al 1997b;Turrin et al 2001). While it appears unlikely that centrally produced cytokines are the exclusive mediators of peripheral LPS anorexia (for review, see Langhans, 2004), they may contribute under certain circumstances.…”

Section: Cytokinesmentioning

confidence: 99%

Signals generating anorexia during acute illness

Langhans

2007

Proc. Nutr. Soc.

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Anorexia is part of the body's acute-phase response to illness. Microbial products such as lipopolysaccharides (LPS), which are also commonly used to model acute illness, trigger the acute-phase response and cause anorexia mainly through pro-inflammatory cytokines. LPS stimulate cytokine production through the cell-surface structural molecule CD14 and toll-like receptor-4. Cytokines ultimately change neural activity in brain areas controlling food intake and energy balance. The blood-brain barrier endothelial cells (BBB EC) are an important site of cytokine action in this context. BBB EC and perivascular cells (microglia and macrophages) form a complex regulatory interface that modulates neuronal activity by the release of messengers (e.g. PG, NO) in response to peripheral challenges. Serotonergic neurons originating in the raphe nuclei and glucagon-like peptide-1-expressing neurons in the hindbrain may be among the targets of these messengers, because serotonin (5-HT), acting through the 5-HT 2C receptor, and glucagon-like peptide-1 have recently emerged as neurochemical mediators of LPS anorexia. The central melanocortin system, which is a downstream target of serotonergic neurons, also appears to be involved in mediation of LPS anorexia. Interestingly, LPS also reduce orexin expression and the activity of orexin neurons in the lateral hypothalamic area of fasted mice. As the eating-stimulatory properties of orexin are apparently related to arousal, the inhibitory effect of LPS on orexin neurons might be involved in LPS-induced inactivity and anorexia. In summary, the immune signalling pathways of LPS-induced, and presumably acute illness-induced, anorexia converge on central neural signalling systems that control food intake and energy balance in healthy individuals.

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Expression of interleukin 1α, interleukin 1β and interleukin 1 receptor antagonist mRNA in mouse brain: regulation by bacterial lipopolysaccharide (LPS) treatment

Cited by 140 publications

References 48 publications

Dietary melatonin selectively reverses age-related changes in cortical cytokine mRNA levels, and their responses to an inflammatory stimulus

Dietary melatonin selectively reverses age-related changes in cortical cytokine mRNA levels, and their responses to an inflammatory stimulus

Inhibition of Tumor Necrosis Factor-α Action within the CNS Markedly Reduces the Plasma Adrenocorticotropin Response to Peripheral Local Inflammation in Rats

Signals generating anorexia during acute illness

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