NDLI: Pro- and anti-inflammatory cytokines regulate the ERK pathway: Implication of the timing for the activation of microglial cells

Content Provider	Springer Nature Link
Author	Saud, Katherine Herrera Molina, Rodrigo Bernhardi, Rommy
Copyright Year	2005
Abstract	Pro-inflammatory molecules induce glial activation and the release of potentially detrimental factors capable of generating oxidative damage, such as nitric oxide (NO) and superoxide anion (O$_{2}$ $^{·−}$. Activated glial cells (astrocytes and microglia) are associated to the inflammatory process in neurodegenerative diseases. A strong inflammatory response could escape endogenous control becoming toxic to neurons and contributing to the course of the disease. We evaluated in a hippocampal cells-microglia co-culture model, if the pro-inflammatory condition induced by lipopolysaccharide + interferon-γ (LPS+IFN-γ) promoted damage directly or if damage was secondary to glial activation. In addition, we explored the effect of the anti-inflammatory cytokine transforming growth factor-β1 (TGF-β1), and pro-inflammatory cytokines, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) on the regulation of the inflammatory response of microglia. We found that LPS+IFN-γ-induced damage on hippocampal cultures was dependent on the presence of microglial cells. In hippocampal cultures exposed to LPS+IFN-γ, TGF-β1 was induced whereas in microglial cell cultures LPS+IFN-γ induced the secretion of IL-1β. TGF-β1 and IL-1β but not TNF-α decreased the NO production by 70–90%. PD98059, an inhibitor of MAP kinase (MEK), reduced the IFN-γ-induced NO production by 40%. TGF-β1 and IL-1β reduced the IFN-γ-induced phosphorylation of ERK1,2 by 60% and 40%, respectively. However, the effect of IL-1β was observed at 30 min and that of TGF-β1 only after 24 h of exposure. We propose that acting with different timing, TGF-β1 and IL-1β can modulate the extracellular signal-regulated kinase ERK1,2, as a common element for different transduction pathways, regulating the amplitude and duration of glial activation in response to LPS+IFN-γ. Cross-talk among brain cells may be key for the understanding of inflammatory mechanisms involved in pathogenesis of neurodegenerative diseases.
Starting Page	277
Ending Page	287
Page Count	11
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	8
Issue Number	3-4
e-ISSN	14763524
Language	English
Publisher	Springer-Verlag
Publisher Date	2005-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Inflammation Cytokines ERK pathway Microglia Lipopolysaccharide Interferon Tumor necrosis factor Interleukins Neurodegeneration Neurosciences Pharmaceutical Sciences/Technology Neurology Neurochemistry Pharmacology/Toxicology Neurobiology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Anti-Inflammatory Role of the Isoflavone Diadzein in Lipopolysaccharide-Stimulated Microglia: Implications for Parkinson’s Disease

Parkinson's disease and inflammatory changes

Neochlorogenic Acid Inhibits Lipopolysaccharide-Induced Activation and Pro-inflammatory Responses in BV2 Microglial Cells

Neuroprotective Effect of Ghrelin in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Mouse Model of Parkinson’s Disease by Blocking Microglial Activation

Angiotensin II AT1 receptor blockade ameliorates brain inflammation.

Doxycycline Suppresses Microglial Activation by Inhibiting the p38 MAPK and NF-kB Signaling Pathways

Glial cell dysregulation: a new perspective on Alzheimer disease

Microglial activation and chronic neurodegeneration

In Vivo Molecular Markers for Pro-inflammatory Cytokine M1 Stage and Resident Microglia in Trimethyltin-Induced Hippocampal Injury

Pro- and anti-inflammatory cytokines regulate the ERK pathway: Implication of the timing for the activation of microglial cells

Similar Documents

Anti-Inflammatory Role of the Isoflavone Diadzein in Lipopolysaccharide-Stimulated Microglia: Implications for Parkinson’s Disease

Parkinson's disease and inflammatory changes

Neochlorogenic Acid Inhibits Lipopolysaccharide-Induced Activation and Pro-inflammatory Responses in BV2 Microglial Cells

Neuroprotective Effect of Ghrelin in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Mouse Model of Parkinson’s Disease by Blocking Microglial Activation

Angiotensin II AT1 receptor blockade ameliorates brain inflammation.

Doxycycline Suppresses Microglial Activation by Inhibiting the p38 MAPK and NF-kB Signaling Pathways

Glial cell dysregulation: a new perspective on Alzheimer disease

Microglial activation and chronic neurodegeneration

In Vivo Molecular Markers for Pro-inflammatory Cytokine M1 Stage and Resident Microglia in Trimethyltin-Induced Hippocampal Injury

Pro- and anti-inflammatory cytokines regulate the ERK pathway: Implication of the timing for the activation of microglial cells