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Experimental sepsis induces sustained inflammation and acetylcholinesterase activity impairment in the hypothalamus

Santos-Junior, N.N. ; Catalão, C.H.R. ; Costa, L.H.A. ; Souza, A.O. ; Mota, C.M.D. ; Alberici, L.C. ; Branco, L.G.S. ; Rocha, M.J.A.

Journal of neuroimmunology, 2018-11, Vol.324, p.143-148 [Periódico revisado por pares]

Netherlands: Elsevier B.V

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  • Título:
    Experimental sepsis induces sustained inflammation and acetylcholinesterase activity impairment in the hypothalamus
  • Autor: Santos-Junior, N.N. ; Catalão, C.H.R. ; Costa, L.H.A. ; Souza, A.O. ; Mota, C.M.D. ; Alberici, L.C. ; Branco, L.G.S. ; Rocha, M.J.A.
  • Assuntos: Acetylcholine ; Cecal ligation and puncture ; Encephalopathy ; Microglia ; Vasopressin
  • É parte de: Journal of neuroimmunology, 2018-11, Vol.324, p.143-148
  • Notas: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
  • Descrição: Sepsis is one of the leading causes of mortality in intensive care units besides causing profound alterations in the brain. One of the structures notably affected during sepsis is the hypothalamus, resulting in important physiopathological consequences. Recently, we provided evidence that the presence of neuroinflammation, oxidative stress, and apoptosis in the hypothalamus of septic rats, is accompanied by impairment of arginine vasopressin (AVP) secretion. We had also demonstrated that sepsis survivor animals present attenuated AVP secretion after osmotic challenge, suggesting a persistent inflammation in the hypothalamus. However, the long-term course of inflammation in the hypothalamus remains unclear. Thus, we induced sepsis by cecal ligation and puncture (CLP) in Wistar rats and, five days after sepsis induction, the hypothalamus of each animal was collected for analysis. Nonmanipulated animals (naive) were used as controls. We found that CLP-induced morphological alterations in microglial cells are accompanied by an increase in Iba-1 immunoreactivity. Moreover, we observed enhanced expression of NF-κB and CREB transcription factors, which are well known to modulate the immune response. Additionally, we found that phosphorylation of GSK3α/β (a kinase upstream to the CREB signaling pathway) was increased, as well as COX-2, iNOS, and IL-6 that are canonic inflammatory proteins. Thus, our results indicated the presence of sustained activation of resident glial cells that may result in neuroinflammation and cholinergic neurotransmission disruptions in the hypothalamus. [Display omitted] •Sepsis causes a persistent microglial activation in the rats hypothalamus.•Immunologic signaling pathways activation in the survivor rats hypothalamus•Increase of hypothalamic inflammatory mediators in sepsis survivors•Decreased cholinergic neurotransmission in the survivor rats hypothalamus.
  • Editor: Netherlands: Elsevier B.V
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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