Study type: In vivo/preclinical · Status: Evidence verified by machine against declared source
VPAC1 receptor (Vipr1)-deficient mice exhibit ameliorated experimental autoimmune encephalomyelitis, with specific deficits in the effector stage.
Journal of neuroinflammation · 2016
Study scale: For antagonist/agonist treatment studies during ongoing EAE, the VPAC1 antagonist PG97-269 at 10 nmol per mouse or the VPAC1 agonist (Ala11, 22, 28)VIP at 5 nmol per mouse were administered i.p. for five consecutive days starting on day 3 after mice immunization with MOG.
Abstract only: Open source record
Product or molecular entity relationships
- VIP: Exact entity relationship. Legacy citation custody associates this source with the catalog record; no product-relevance conclusion is implied.
Public plain-language summary
Some fields are not published, because the text held for them did not answer their heading. The published text is limited to the declared source and preserves reported uncertainty. It does not establish efficacy, safety, suitability, or evidence strength.
Research question
Here, we investigated the involvement of VPAC1 in the development of EAE using a VPAC1-deficient mouse model.
Study design
In vitro and ex vivo experiments repeatedly demonstrate that these peptides exert pronounced immunomodulatory (primarily anti-inflammatory) actions which are mediated by common VPAC1 and VPAC2 G protein-coupled receptors.
Participants or experimental system
EAE was induced in wild-type (WT) and VPAC1 knockout (KO) mice using myelin oligodendrocyte glycoprotein 35–55 (MOG35–55), and clinical scores were assessed continuously over 30 days.
Study scale
For antagonist/agonist treatment studies during ongoing EAE, the VPAC1 antagonist PG97-269 at 10 nmol per mouse or the VPAC1 agonist (Ala11, 22, 28)VIP at 5 nmol per mouse were administered i.p. for five consecutive days starting on day 3 after mice immunization with MOG.
Intervention or exposure
The immunization phase of EAE appeared to be unimpaired because lymph node cells from EAE-induced VPAC1 KO mice stimulated in vitro with MOG exhibited robust proliferative and Th1/Th17 responses.
Comparator
MOG35–55-induced EAE was ameliorated in VPAC1 KO mice compared to WT mice.
Outcomes examined
The contribution of VPAC1 expression in the immune system to the development of EAE was evaluated by means of adoptive transfer and bone marrow chimera experiments.
Key findings
In agreement, we have shown that mice deficient in PACAP ligand or VPAC2 receptors exhibit exacerbated experimental autoimmune encephalomyelitis (EAE).
Limitations and uncertainty
Not published. The text held for this field did not answer this heading, so nothing is shown here and nothing is substituted for it.
Product relevance and evidence boundary
This record is a published study, held here with its citation and review status. It is not a statement that any catalog item is effective, safe, or suitable for any use, and nothing in it is a dose or a protocol.
Evidence verified by machine against declared source. Verification is limited to the declared source and review scope. It does not mean independent replication or establish efficacy, safety, or suitability.