Macrophage inflammatory protein-1: Unique action on the hypothalamus to evoke fever

Miñano, F.J.; Sancibrián, M.; Vizcaino, Maricarmen; Páez, Ximena; Davatelis, G.; Fahey, Thomas J.; Sherry, Barbara; Cerami, Anthony; Myers, R.D.

doi:10.1016/0361-9230(90)90150-x

Cited by 71 publications

(38 citation statements)

References 24 publications

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“…Indeed, in view of this, the intriguing possibility exists that, in contrast to PGE 2 generated in the liver (39,55,75), PGE 2 in the POA, however it may occur there, may not be essential to the production of fever. The independence of febrigenesis from central PGE 2 has been reported previously in connection with certain pyrogenic cytokines, e.g., macrophage inflammatory protein-1␤ (38,47), , and preformed pyrogenic factor (86); the fever, in those cases, was attributed to the direct action of the cytokines in the POA.…”

Section: Discussionsupporting

confidence: 59%

Preoptic nitric oxide attenuates endotoxic fever in guinea pigs by inhibiting the POA release of norepinephrine

Feleder¹,

Perlik²,

Blatteis³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Lipopolysaccharide (LPS) administration induces hypothalamic nitric oxide (NO); NO is antipyretic in the preoptic area (POA), but its mechanism of action is uncertain. LPS also stimulates the release of preoptic norepinephrine (NE), which mediates fever onset. Because NE upregulates NO synthases and NO induces cyclooxygenase (COX)-2-dependent PGE2, we investigated whether NO mediates the production of this central fever mediator. Conscious guinea pigs with intra-POA microdialysis probes received LPS intravenously (2 μg/kg) and, thereafter, an NO donor (SIN-1) or scavenger (carboxy-PTIO) intra-POA (20 μg/μl each, 2 μl/min, 6 h). Core temperature (Tc) was monitored constantly; dialysate NE and PGE2 were analyzed in 30-min collections. To verify the reported involvement of α2-adrenoceptors (AR) in PGE2 production, clonidine (α2-AR agonist, 2 μg/μl) was microdialyzed with and without SIN-1 or carboxy-PTIO. To assess the possible involvement of oxidative NE and/or NO products in the demonstrated initially COX-2-independent POA PGE2 increase, (+)-catechin (an antioxidant, 3 μg/μl) was microdialyzed, and POA PGE2, and Tc were determined. SIN-1 and carboxy-PTIO reduced and enhanced, respectively, the rises in NE, PGE2, and Tc produced by intravenous LPS. Similarly, they prevented and increased, respectively, the delayed elevations of PGE2 and Tc induced by intra-POA clonidine. (+)-Catechin prevented the LPS-induced elevation of PGE2, but not of Tc. We conclude that the antipyretic activity of NO derives from its inhibitory modulation of the LPS-induced release of POA NE. These data also implicate free radicals in POA PGE2 production and raise questions about its role as a central LPS fever mediator.

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Section: Discussionsupporting

confidence: 59%

Preoptic nitric oxide attenuates endotoxic fever in guinea pigs by inhibiting the POA release of norepinephrine

Feleder¹,

Perlik²,

Blatteis³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Indeed, injections of IL-8/CXCL8, macrophage inflammatory protein-1 alpha and beta (MIP-1a/CCL3 and MIP1b/CCL4), and RANTES/CCL5 induce hyperthermia. It was observed that MIP-1a/CCL3 and MIP-1b/CCL4 administered intravenously in the rabbit or into the anterior hypothalamic/preoptic area (AH/POA), a region containing thermosensitive neurons in the rat, evoke a dose-dependent febrile response characteristic of endogenous pyrogen (Davatelis et al 1989, Minano et al 1990, 1991a. It was reported that these two chemokines present differences in their ability to induce hyperthermia.…”

Section: Chemokines and Body Temperaturementioning

confidence: 99%

Chemokines and chemokine receptors in the brain: implication in neuroendocrine regulation

Callewaere

Banisadr²,

Rostène³

et al. 2007

Journal of Molecular Endocrinology

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Chemokines are small secreted proteins that chemoattract and activate immune and non-immune cells both in vivo and in vitro. In addition to their well-established role in the immune system, several recent reports have suggested that chemokines and their receptors may also play a role in the central nervous system (CNS). The best known central action is their ability to act as immuno-inflammatory mediators. Indeed, these proteins regulate leukocyte infiltration in the brain during inflammatory and infectious diseases. However, we and others recently demonstrated that they are expressed not only in neuroinflammatory conditions, but also constitutively by different cell types including neurons in the normal brain, suggesting that they may act as modulators of neuronal functions. The goal of this review is to highlight the role of chemokines in the control of neuroendocrine functions. First, we will focus on the expression of chemokines and their receptors in the CNS, with the main spotlight on the neuronal expression in the hypothalamo-pituitary system. Secondly, we will discuss the role -we can now suspect -of chemokines and their receptors in the regulation of neuroendocrine functions. In conclusion, we propose that chemokines can be added to the well-described neuroendocrine regulatory mechanisms, providing an additional fine modulatory tuning system in physiological conditions.

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“…Many of these cytokines, including interleukin (IL)-I, IL-6, tumour necrosis factor-cz (TNF-z), interferons (IFNs), and macrophage inflammatory protein-1 (MIP-1), generally known as endogenous pyrogens (EPs), can induce fever when injected into experimental animals and humans. [1][2][3][4][5] It is likely that IL-1, IL-6, TNF-x and IFNs induce fever by stimulating synthesis of prostaglandins (PGs). On the other hand, fevers induced by MIP-1 in rabbits and rats and IL-8 in rats are independent of prostaglandin synthesis.…”

Section: Introductionmentioning

confidence: 99%

“…On the other hand, fevers induced by MIP-1 in rabbits and rats and IL-8 in rats are independent of prostaglandin synthesis. [2][3][4][5] Another important component of APR is neutrophilia, which is also dependent on synthesis and release of cytokines, including IL-Iz and [3, TNF-cz and IL-6, IL-8, as well other inflammatory mediators 6 11 such as C5a and PGs (El, Ei, Fzcz).…”

Section: Introductionmentioning

confidence: 99%

Effects of anti‐inflammatory drugs on fever and neutrophilia induced by Clostridium difficile toxin B

Cardoso

Filho

Júnior

et al. 1996

Mediators of Inflammation

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Macrophage inflammatory protein-1: Unique action on the hypothalamus to evoke fever

Cited by 71 publications

References 24 publications

Preoptic nitric oxide attenuates endotoxic fever in guinea pigs by inhibiting the POA release of norepinephrine

Preoptic nitric oxide attenuates endotoxic fever in guinea pigs by inhibiting the POA release of norepinephrine

Chemokines and chemokine receptors in the brain: implication in neuroendocrine regulation

Effects of anti‐inflammatory drugs on fever and neutrophilia induced by Clostridium difficile toxin B

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