Evidence map›Paper›PMID 24659539›Full record

ArticleGlia2014

LPS and IL-1 differentially activate mouse and human astrocytes: role of CD14.

Leonid Tarassishin, Hyeon-Sook Suh, Sunhee C Lee

Abstract readComparative Study
In one paragraph

Article in Glia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

124 citing papers in PubMed, 209 citations in OpenAlex.

  1. Article
  2. Article
  3. LPS-induced inflammation differentially affects endogenous CaMolecular medicine (Cambridge, Mass.) · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Astrocytes as Therapeutic Targets in Neurodegenerative Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. DAMPs Drive Fibroinflammatory Changes in the Glaucomatous ONH.Investigative ophthalmology & visual science · 2024
    Article

64 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Leonid TarassishinDepartment of Pathology, Albert Einstein College of Medicine, Bronx, New York, 10461.
Hyeon-Sook Suh
Sunhee C Lee
Albert Einstein College of Medicine · US

Funding

Immunology/Pathology CoreP30AI051519 · NIAID · YESHIVA UNIVERSITY · PI GOLDSTEIN, HARRIS · 2003 to 2013
$18.6M
Molecular NeuropathologyT32NS007098 · NINDS · YESHIVA UNIVERSITY · PI SANTAMBROGIO, LAURA · 1985 to 2015
$5.0M
Microglia, Cytokines and HIVR01MH055477 · NIMH · YESHIVA UNIVERSITY · PI LEE, SUNHEE C · 1995 to 2011
$4.1M
NIAID NIH HHS P30 AI051519NIMH NIH HHS R01 MH055477NIMH NIH HHS R01 MH55477NINDS NIH HHS T32 NS007098
6 · The paper itself

Abstract

Treatment of cultures with toll-like receptor (TLR) ligands or cytokines has become a popular approach to investigate astrocyte neuroinflammatory responses and to simulate the neural environment in various CNS disorders. However, despite much effort, the mechanism of astrocyte activation such as their responses to the TLR ligands and IL-1 remain highly debated. We compared highly pure primary mouse and human astrocyte cultures in their ability to produce proinflammatory mediators (termed "A1") and immunoregulatory mediators (termed "A2") in response to LPS, poly IC, and IL-1 stimulation. In human astrocytes, IL-1 induced both A1 and A2 responses, poly IC induced mostly A2, and LPS induced neither. In mouse astrocytes, LPS induced mostly an A1-predominant response, poly IC induced both A1 and A2, and IL-1 neither. In addition, mouse astrocytes produce abundant IL-1 protein, whereas human astrocytes did not, despite robust IL-1 mRNA expression. Of the TLR4 receptor complex proteins, human astrocytes expressed TLR4 and MD2 but not CD14, whereas mouse astrocytes expressed all three. Mouse astrocyte CD14 (cell-associated and soluble) was potently upregulated by LPS. Silencing TLR4 or CD14 by siRNA suppressed LPS responses in mouse astrocytes. In vivo, astrocytes in LPS-injected mouse brains also expressed CD14. Our results show striking differences between human and mouse astrocytes in the use of TLR/IL-1R and subsequent downstream signaling and immune activation. IL-1 translational block in human astrocytes may be a built-in mechanism to prevent autocrine and paracrine cell activation and neuroinflammation. These results have important implications for translational research of human CNS diseases.

Indexed as

AnimalsAnimals, NewbornAstrocytesCells, CulturedFetusHumansInterleukin-1Lipopolysaccharide ReceptorsLipopolysaccharidesMiceMice, Inbred C57BLSpecies SpecificityInterleukin-1Lipopolysaccharide ReceptorsLipopolysaccharidesbraincytokinesevolutioninflammationinnate immunitypoly ICspeciesTLR

Identifiers

PMID24659539
PMCPMC4015139
OpenAlexW2103901522

What OpenQuestion holds

Textmetadata
LicenceTDM
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.