Temporal and spatial relationships between lipopolysaccharide-induced expression of fos, interleukin-1 β and inducible nitric oxide synthase in rat brain

@article{Konsman1999TemporalAS,
  title={Temporal and spatial relationships between lipopolysaccharide-induced expression of fos, interleukin-1 $\beta$ and inducible nitric oxide synthase in rat brain},
  author={Jan Pieter Konsman and Keith W. Kelley and Robert Dantzer},
  journal={Neuroscience},
  year={1999},
  volume={89},
  pages={535-548}
}
Rat brain vascular distribution of interleukin‐1 type‐1 receptor immunoreactivity: Relationship to patterns of inducible cyclooxygenase expression by peripheral inflammatory stimuli
TLDR
Observations indicate that functional IL‐1R1s are expressed in endothelial cells of brain venules and suggest that vascular IL‐ 1R1 distribution is an important factor determining BBB prostaglandin‐dependent activation of brain structures during infection.
Central nervous action of interleukin‐1 mediates activation of limbic structures and behavioural depression in response to peripheral administration of bacterial lipopolysaccharide
TLDR
Findings can be interpreted to suggest that circulating or locally produced brain IL‐1β acts on these cells to bring about behavioural depression and activation of limbic structures during the APR after peripheral LPS administration.
Brain Perivascular Macrophages Do Not Mediate Interleukin-1-Induced Sickness Behavior in Rats
TLDR
It is shown that intracerebroventricular administration of an IL-1β-saporin conjugate is an efficient way to target brain perivascular macrophages, and to determine whether these cells are involved in IL- 1β-induced sickness behavior.
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It is demonstrated that LPS stimulates hypothalamic CRH by a mechanism that involves the action of IL-1 within the central nervous system and may proceed independently of peripheral actions ofIL-1 circulating in the bloodstream.
Distribution of fos‐like immunoreactivity in the rat brain following intravenous lipopolysaccharide administration
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A significant sustained elevation of Fos‐like immunoreactivity was observed in a cell group adjacent to the organum vasculosum of the lamina terminalis, which is lead to hypothesize that the ventromedial preoptic area may be a key site for the initiation of fever during endotoxemia.
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It is proposed that the vascular and peri-vascular induction of iNOS mRNA by IL-1 beta might represent a mechanism for the modulation of the central nervous system effects of peripheral inflammatory mediators.
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TLDR
Data indicate that following systemic administration, IL-1 beta may activate specific brain areas through mechanisms distinct from those involved following central administration, and Physiologically, these results suggest that IL- 1 beta may have differential central effects depending on its source or point of entry to the brain.
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TLDR
Rats injected with both LPS and IL-1ra showed decreased hepatic iNOS mRNA and plasma NO2- + NO3- compared with rats given LPS alone, indicating thatIL-1 beta plays a role in regulating iN OS expression within the liver in vivo during endotoxemia.
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TLDR
The functional neuroanatomy of the immune system link to the CNS was investigated by assessing neuronal activity with Fos immunohistochemistry following systemic lipopolysaccharide (LPS) administration and image analysis was utilized to quantify the Fos induction in the CNS.
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