Peripheral origin of IL-1Β production in the rodent hippocampus under in vivo systemic bacterial lipopolysaccharide (LPS) challenge and its regulation by P2X7 receptors

C. Csölle, B. Sperlágh

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

In this study we showed that in vivo bacterial lipopolysaccharide (LPS) challenge elevated IL-1Β level in the rodent hippocampus. Antagonists of P2X receptors inhibited LPS-induced IL-1Β level with a pharmacological profile similar to that of P2X7R and their inhibitory effect was attenuated in the absence of P2X7R. In wild-type mice, LPS overexpressed mRNA encoding P2X4 and P2X7 receptors in the hippocampus and caused also a remarkable increase in the levels of IL-1Β in the serum. The hippocampal increase of IL-1Β has substantially alleviated when contamination of circulating blood cells was excluded by transcardial perfusion, indicating the peripheral origin of hippocampal IL-1Β elevation. These results point to the key role of the endogenous activation of peripheral P2X7R in the level of IL-1Β in rodent hippocampus under systemic bacterial endotoxin challenge.

Original languageEnglish
Pages (from-to)38-46
Number of pages9
JournalJournal of Neuroimmunology
Volume219
Issue number1-2
DOIs
Publication statusPublished - Feb 2010

Fingerprint

Purinergic P2X7 Receptors
Interleukin-1
Lipopolysaccharides
Rodentia
Hippocampus
Purinergic P2X4 Receptors
CD14 Antigens
Endotoxins
Blood Cells
Perfusion
Pharmacology
Messenger RNA
Serum

Keywords

  • Hippocampus
  • IL-1Β
  • In vivo
  • LPS
  • P2XR

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

Cite this

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title = "Peripheral origin of IL-1Β production in the rodent hippocampus under in vivo systemic bacterial lipopolysaccharide (LPS) challenge and its regulation by P2X7 receptors",
abstract = "In this study we showed that in vivo bacterial lipopolysaccharide (LPS) challenge elevated IL-1Β level in the rodent hippocampus. Antagonists of P2X receptors inhibited LPS-induced IL-1Β level with a pharmacological profile similar to that of P2X7R and their inhibitory effect was attenuated in the absence of P2X7R. In wild-type mice, LPS overexpressed mRNA encoding P2X4 and P2X7 receptors in the hippocampus and caused also a remarkable increase in the levels of IL-1Β in the serum. The hippocampal increase of IL-1Β has substantially alleviated when contamination of circulating blood cells was excluded by transcardial perfusion, indicating the peripheral origin of hippocampal IL-1Β elevation. These results point to the key role of the endogenous activation of peripheral P2X7R in the level of IL-1Β in rodent hippocampus under systemic bacterial endotoxin challenge.",
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AU - Sperlágh, B.

PY - 2010/2

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N2 - In this study we showed that in vivo bacterial lipopolysaccharide (LPS) challenge elevated IL-1Β level in the rodent hippocampus. Antagonists of P2X receptors inhibited LPS-induced IL-1Β level with a pharmacological profile similar to that of P2X7R and their inhibitory effect was attenuated in the absence of P2X7R. In wild-type mice, LPS overexpressed mRNA encoding P2X4 and P2X7 receptors in the hippocampus and caused also a remarkable increase in the levels of IL-1Β in the serum. The hippocampal increase of IL-1Β has substantially alleviated when contamination of circulating blood cells was excluded by transcardial perfusion, indicating the peripheral origin of hippocampal IL-1Β elevation. These results point to the key role of the endogenous activation of peripheral P2X7R in the level of IL-1Β in rodent hippocampus under systemic bacterial endotoxin challenge.

AB - In this study we showed that in vivo bacterial lipopolysaccharide (LPS) challenge elevated IL-1Β level in the rodent hippocampus. Antagonists of P2X receptors inhibited LPS-induced IL-1Β level with a pharmacological profile similar to that of P2X7R and their inhibitory effect was attenuated in the absence of P2X7R. In wild-type mice, LPS overexpressed mRNA encoding P2X4 and P2X7 receptors in the hippocampus and caused also a remarkable increase in the levels of IL-1Β in the serum. The hippocampal increase of IL-1Β has substantially alleviated when contamination of circulating blood cells was excluded by transcardial perfusion, indicating the peripheral origin of hippocampal IL-1Β elevation. These results point to the key role of the endogenous activation of peripheral P2X7R in the level of IL-1Β in rodent hippocampus under systemic bacterial endotoxin challenge.

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