This study examines the role of a central pathway involving glutamate receptors, nitric oxide (NO) and cGMP in the acute inhibitory effects of central interleukin 1beta on pentagastrin-stimulated acid production.The acid-inhibitory effect of central interleukin 1beta was prevented by intracisternal (i.c.) microinjections of interleukin 1beta together with the NMDA receptor antagonist, dizocilpine maleate (MK-801). Intracisternal co-administration of the nitric oxide synthase inhibitor, N(G)-nitro- L-arginine methyl esther ( L-NAME) or 1H-[1,2,4]oxazodiolo[4,3-a]quinoxalin-1-one (ODQ), a soluble guanylyl cyclase (sGC) blocker, both reversed the hyposecretory effect of central interleukin 1beta. Peripheral administration of endotoxin significantly reduced pentagastrin-stimulated gastric acid secretion. I.c. pre-treatment with the interleukin 1 receptor antagonist, IL-1ra, failed to restore acid secretory responses in these rats. In addition, endotoxin did not modify the levels of endogenous mRNA for IL-1beta in the brainstem. We conclude that central glutamate receptors are involved in the acid inhibitory effect of centrally administered interleukin 1beta. This central pathway involves synthesis of NO, which acts on the enzyme sGC. However, endogenous interleukin 1beta does not seem to be involved in the inhibition of gastric acid secretion elicited by peripheral endotoxin.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s00210-002-0654-7 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Distinct peripheral pro-inflammatory profile associated with tuberous sclerosis complex and epilepsy.
Epilepsia
January 2025
Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montreal, Quebec, Canada.
Objective: Tuberous sclerosis complex (TSC) is a monogenetic disorder associated with sustained mechanistic target of rapamycin (mTOR) activation, leading to heterogeneous clinical manifestations. Epilepsy and renal angiomyolipoma are the most important causes of morbidity in adult people with TSC (pwTSC). mTOR is a key player in inflammation, which in turn could influence TSC-related clinical manifestations.
View Article and Find Full Text PDFCorrelation of fecal microbiome dysregulation to synovial transcriptome in an equine model of obesity associated osteoarthritis.
Ann Transl Med
December 2024
Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, USA.
Background: Osteoarthritis (OA) is increasingly thought to be a multifactorial disease in which sustained gut inflammation serves as a continued source of inflammatory mediators driving degenerative processes at distant sites such as joints. The objective of this study was to use the equine model of naturally occurring obesity associated OA to compare the fecal microbiome in OA and health and correlate those findings to differential gene expression synovial fluid (SF) cells, circulating leukocytes and cytokine levels (plasma, SF) towards improved understanding of the interplay between microbiome and immune transcriptome in OA pathophysiology.
Methods: Feces, peripheral blood mononuclear cells (PBMCs), and SF cells were isolated from healthy skeletally mature horses (n=12; 6 males, 6 females) and those with OA (n=6, 2 females, 4 males).
Intra-articular injection of inorganic pyrophosphate improves IL-1β-induced cartilage damage in rat model of knee osteoarthritis in vivo.
Osteoarthr Cartil Open
March 2025
Université de Lorraine, CNRS (French National Centre for Scientific Research), IMoPA (Molecular Engineering and Articular Physiopathology), F-54000, Nancy, France.
Objective: Osteoarthritis (OA) is the most common form of chronic joint disease, affecting mainly the elderly population. This disorder is caused by cartilage degeneration with complex changes in the chondrocyte phenotype. Inorganic pyrophosphate (PPi) was shown to counteract the detrimental effect of interleukin (IL)-1β challenging in an in vitro OA model based on rat articular chondrocytes.
View Article and Find Full Text PDFLipopolysaccharide-Neutralizing Peptide Modulates P2X7 Receptor-Mediated Interleukin-1β Release.
ACS Pharmacol Transl Sci
January 2025
Pharmaceutical Institute, Pharmacology and Toxicology, University of Bonn, Gerhard-Domagk-Str. 3, 53121 Bonn, Germany.
Lipopolysaccharide (LPS)-neutralizing peptides are emerging as new potential therapeutic modalities to treat sepsis and skin infections. Purinergic ligand-gated ion channels (P2X receptors) play a critical role in various biological processes, including inflammation. Recent drug development efforts have significantly focused on the modulation of P2X receptors.
View Article and Find Full Text PDFNeuroprotective and inflammatory biomarkers in pediatric drug-resistant epilepsy: Interplay between GDNF, IL-1β and vitamin D 25-OH.
Narra J
December 2024
Department of Clinical Pathology, Faculty of Medicine, Universitas Imelda, Medan, Indonesia.
Drug-resistant epilepsy in pediatric patients is associated with neuroinflammation and neurodegeneration. Vitamin D 25-OH exerts neuroprotective effects, while glial cell line- derived neurotrophic factor (GDNF) and the proinflammatory cytokine interleukin-1β (IL-1β) are implicated in the mechanisms of neuroinflammation and epileptogenesis. The aim of this study was to investigate the relationship between vitamin D 25-OH, IL-1β, and GDNF levels with seizure severity and frequency in children with drug-resistant epilepsy.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!