Evidence map›Paper›PMID 18523290›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Neurogenic exacerbation of microglial and astrocyte responses to Neisseria meningitidis and Borrelia burgdorferi.

Vinita S Chauhan, David G Sterka, David L Gray, Kenneth L Bost, Ian Marriott

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
2.2field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
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  9. Substance P-Friend or Foe.Journal of clinical medicine · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Vinita S ChauhanDepartment of Biology, University of North Carolina, Charlotte, NC 28223, USA.
David G Sterka
David L Gray
Kenneth L Bost
Ian Marriott
University of North Carolina at Charlotte · US

Funding

Substance P exacerbation of CNS inflammationR01NS050325 · NINDS · UNIVERSITY OF NORTH CAROLINA CHARLOTTE · PI MARRIOTT, IAN, PHILIPP, MARIO TOMAS · 2006 to 2016
$3.6M
Novel intracellular pattern recognition receptor expression by resident CNS cellsR03NS057434 · NINDS · UNIVERSITY OF NORTH CAROLINA CHARLOTTE · PI MARRIOTT, IAN · 2007 to 2009
$209k
NINDS NIH HHS NS 050325NINDS NIH HHS NS 057434NINDS NIH HHS R01 NS050325NINDS NIH HHS R03 NS057434
6 · The paper itself

Abstract

Although glial cells are recognized for their roles in maintaining neuronal function, there is growing appreciation of the ability of resident CNS cells to initiate and/or augment inflammation following trauma or infection. The tachykinin, substance P (SP), is well known to augment inflammatory responses at peripheral sites and its presence throughout the CNS raises the possibility that this neuropeptide might serve a similar function within the brain. In support of this hypothesis, we have recently demonstrated the expression of high affinity receptors for SP (Neurokinin-1 (NK-1) receptors) on microglia and shown that this tachykinin can significantly elevate bacterially induced inflammatory prostanoid production by isolated cultures of these cells. In the present study, we demonstrate that endogenous SP/NK-1R interactions are an essential component in the initiation and/or progression of CNS inflammation in vivo following exposure to two clinically relevant bacterial CNS pathogens, Neisseria meningitidis and Borrelia burgdorferi. We show that in vivo elevations in inflammatory cytokine production and decreases in the production of an immunosuppressive cytokine are markedly attenuated in mice genetically deficient in the expression of the NK-1R or in mice treated with a specific NK-1R antagonist. Furthermore, we have used isolated cultures of microglia and astrocytes to demonstrate that SP can augment inflammatory cytokine production by these resident CNS cell types following exposure to either of these bacterial pathogens. Taken together, these studies indicate a potentially important role for neurogenic exacerbation of resident glial immune responses in CNS inflammatory diseases, such as bacterial meningitis.

Indexed as

Borrelia burgdorferiNeisseria meningitidisAnimalsAstrocytesCells, CulturedCytokinesDemyelinating DiseasesGliosisInflammation MediatorsInjections, IntraventricularMeningitis, BacterialMiceMice, Inbred C57BLMice, KnockoutMicrogliaReceptors, Neurokinin-1CytokinesInflammation MediatorsReceptors, Neurokinin-1Substance P

Identifiers

PMID18523290
PMCPMC2507752
OpenAlexW1601132847

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.