Induction of nitric oxide synthase and interleukin-1beta, but not heme oxygenase, messenger RNA in rat brain following peripheral administration of endotoxin.

Previous studies have suggested that both nitric oxide (NO) and carbon monoxide (CO) are important modulators of the inflammatory response, while more recent data have implicated both gases as regulators of hypothalamic neuroendocrine function, particularly the hypothalamo-pituitary-adrenal axis. We...

Full description

Bibliographic Details
Main Authors: Jacobs, R, Satta, M, Dahia, P, Chew, S, Grossman, AB
Format: Journal article
Language:English
Published: 1997
_version_ 1797099197245161472
author Jacobs, R
Satta, M
Dahia, P
Chew, S
Grossman, AB
author_facet Jacobs, R
Satta, M
Dahia, P
Chew, S
Grossman, AB
author_sort Jacobs, R
collection OXFORD
description Previous studies have suggested that both nitric oxide (NO) and carbon monoxide (CO) are important modulators of the inflammatory response, while more recent data have implicated both gases as regulators of hypothalamic neuroendocrine function, particularly the hypothalamo-pituitary-adrenal axis. We have, therefore, investigated the modulation of the transcripts for the synthetic enzymes for both NO and CO following the intraperitoneal administration of lipopolysaccharide, serotype B5 055, over the course of 24 h. The mRNA for type I or neuronal nitric oxide synthase (nNOS), and type II or inducible (iNOS), and heme oxygenase1 ('inducible') and heme oxygenase2 ('constitutive'), were reverse transcribed to cDNA, amplified by the polymerase chain reaction, and then quantified using a co-amplified internal standard, beta-actin. This allowed for assessment of relative changes in transcript concentration. In addition, these were compared to changes in expression of the cytokine, IL-1beta. Finally, absolute levels of the synthetic enzyme transcripts were assessed by means of co-amplification in the presence of varying amounts of mutant templates in a competitive PCR reaction. Our data revealed rapid induction of IL-1beta, iNOS and HO1 in the liver, returning to baseline at 24 h. In the hypothalamus, all transcripts were present under basal conditions, but only IL-1beta and iNOS were induced by the LPS. We conclude that hypothalamic IL-1beta and iNOS can be induced by a non-lethal dose of endotoxin, and are, thus, in a position to mediate certain of the neuroendocrine consequences to inflammatory stress.
first_indexed 2024-03-07T05:20:17Z
format Journal article
id oxford-uuid:dea439ef-ff9e-405e-9b23-9fa9471f14f3
institution University of Oxford
language English
last_indexed 2024-03-07T05:20:17Z
publishDate 1997
record_format dspace
spelling oxford-uuid:dea439ef-ff9e-405e-9b23-9fa9471f14f32022-03-27T09:33:45ZInduction of nitric oxide synthase and interleukin-1beta, but not heme oxygenase, messenger RNA in rat brain following peripheral administration of endotoxin.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:dea439ef-ff9e-405e-9b23-9fa9471f14f3EnglishSymplectic Elements at Oxford1997Jacobs, RSatta, MDahia, PChew, SGrossman, ABPrevious studies have suggested that both nitric oxide (NO) and carbon monoxide (CO) are important modulators of the inflammatory response, while more recent data have implicated both gases as regulators of hypothalamic neuroendocrine function, particularly the hypothalamo-pituitary-adrenal axis. We have, therefore, investigated the modulation of the transcripts for the synthetic enzymes for both NO and CO following the intraperitoneal administration of lipopolysaccharide, serotype B5 055, over the course of 24 h. The mRNA for type I or neuronal nitric oxide synthase (nNOS), and type II or inducible (iNOS), and heme oxygenase1 ('inducible') and heme oxygenase2 ('constitutive'), were reverse transcribed to cDNA, amplified by the polymerase chain reaction, and then quantified using a co-amplified internal standard, beta-actin. This allowed for assessment of relative changes in transcript concentration. In addition, these were compared to changes in expression of the cytokine, IL-1beta. Finally, absolute levels of the synthetic enzyme transcripts were assessed by means of co-amplification in the presence of varying amounts of mutant templates in a competitive PCR reaction. Our data revealed rapid induction of IL-1beta, iNOS and HO1 in the liver, returning to baseline at 24 h. In the hypothalamus, all transcripts were present under basal conditions, but only IL-1beta and iNOS were induced by the LPS. We conclude that hypothalamic IL-1beta and iNOS can be induced by a non-lethal dose of endotoxin, and are, thus, in a position to mediate certain of the neuroendocrine consequences to inflammatory stress.
spellingShingle Jacobs, R
Satta, M
Dahia, P
Chew, S
Grossman, AB
Induction of nitric oxide synthase and interleukin-1beta, but not heme oxygenase, messenger RNA in rat brain following peripheral administration of endotoxin.
title Induction of nitric oxide synthase and interleukin-1beta, but not heme oxygenase, messenger RNA in rat brain following peripheral administration of endotoxin.
title_full Induction of nitric oxide synthase and interleukin-1beta, but not heme oxygenase, messenger RNA in rat brain following peripheral administration of endotoxin.
title_fullStr Induction of nitric oxide synthase and interleukin-1beta, but not heme oxygenase, messenger RNA in rat brain following peripheral administration of endotoxin.
title_full_unstemmed Induction of nitric oxide synthase and interleukin-1beta, but not heme oxygenase, messenger RNA in rat brain following peripheral administration of endotoxin.
title_short Induction of nitric oxide synthase and interleukin-1beta, but not heme oxygenase, messenger RNA in rat brain following peripheral administration of endotoxin.
title_sort induction of nitric oxide synthase and interleukin 1beta but not heme oxygenase messenger rna in rat brain following peripheral administration of endotoxin
work_keys_str_mv AT jacobsr inductionofnitricoxidesynthaseandinterleukin1betabutnothemeoxygenasemessengerrnainratbrainfollowingperipheraladministrationofendotoxin
AT sattam inductionofnitricoxidesynthaseandinterleukin1betabutnothemeoxygenasemessengerrnainratbrainfollowingperipheraladministrationofendotoxin
AT dahiap inductionofnitricoxidesynthaseandinterleukin1betabutnothemeoxygenasemessengerrnainratbrainfollowingperipheraladministrationofendotoxin
AT chews inductionofnitricoxidesynthaseandinterleukin1betabutnothemeoxygenasemessengerrnainratbrainfollowingperipheraladministrationofendotoxin
AT grossmanab inductionofnitricoxidesynthaseandinterleukin1betabutnothemeoxygenasemessengerrnainratbrainfollowingperipheraladministrationofendotoxin