Evidence map›Paper›PMID 26355912›Full record

ArticleMolecular immunology2015

Galectins regulate the inflammatory response in airway epithelial cells exposed to microbial neuraminidase by modulating the expression of SOCS1 and RIG1.

Mihai Nita-Lazar, Aditi Banerjee, Chiguang Feng, Gerardo R Vasta

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

31 citing papers in PubMed, 56 citations in OpenAlex.

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  12. Manipulating Galectin Expression in Zebrafish (Danio rerio).Methods in molecular biology (Clifton, N.J.) · 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

4 authors at 2 institutions in 1 country.

Mihai Nita-LazarDepartment of Microbiology and Immunology, University of Maryland School of Medicine, and Institute of Marine and Environmental Technology, Columbus Center, 701 East Pratt Street, Baltimore, MD 21202, USA.
Aditi BanerjeeDepartment of Microbiology and Immunology, University of Maryland School of Medicine, and Institute of Marine and Environmental Technology, Columbus Center, 701 East Pratt Street, Baltimore, MD 21202, USA.
Chiguang FengDepartment of Microbiology and Immunology, University of Maryland School of Medicine, and Institute of Marine and Environmental Technology, Columbus Center, 701 East Pratt Street, Baltimore, MD 21202, USA.
Gerardo R VastaDepartment of Microbiology and Immunology, University of Maryland School of Medicine, and Institute of Marine and Environmental Technology, Columbus Center, 701 East Pratt Street, Baltimore, MD 21202, USA. Electronic address: GVasta@som.umaryland.edu.
Columbus Center · USUniversity of Maryland, Baltimore · US

Funding

Biological Roles of GalectinsR01GM070589 · NIGMS · UNIVERSITY OF MD BIOTECHNOLOGY INSTITUTE · PI VASTA, GERARDO RAUL · 2004 to 2013
$2.0M
NIGMS NIH HHS 5R01GM070589-06NIGMS NIH HHS R01 GM070589
6 · The paper itself

Abstract

Influenza patients frequently display increased susceptibility to Streptococcus pneumoniae co-infection and sepsis, the prevalent cause of mortality during influenza pandemics. However, the detailed mechanisms by which an influenza infection predisposes patients to suffer pneumococcal pneumonia are not fully understood. A murine model for influenza infection closely reflects the observations in human patients, since if the animals that have recovered from influenza A virus (IAV) sublethal infection are challenged with S. pneumoniae, they undergo a usually fatal uncontrolled cytokine response. We have previously demonstrated both in vitro and in vivo that the expression and secretion of galectin-1 (Gal1) and galectin-3 (Gal3) are modulated during IAV infection, and that the viral neuraminidase unmasks galactosyl moieties in the airway epithelia. In this study we demonstrate in vitro that the binding of secreted Gal1 and Gal3 to the epithelial cell surface modulates the expression of SOCS1 and RIG1, and activation of ERK, AKT or JAK/STAT1 signaling pathways, leading to a disregulated expression and release of pro-inflammatory cytokines. Our results suggest that the activity of the viral and pneumococcal neuraminidases on the surface of the airway epithelial cells function as a "danger signal" that leads to rapid upregulation of SOCS1 expression to prevent an uncontrolled inflammatory response. The binding of extracellular Gal1 or Gal3 to the galactosyl moieties unmasked on the surface of airway epithelial cells can either "fine-tune" or severely disregulate this process, respectively, the latter potentially leading to hypercytokinemia.

Indexed as

AnimalsBacterial ProteinsCell Line, TumorCytokinesDEAD Box Protein 58DEAD-box RNA HelicasesEpithelial CellsEscherichia coliExtracellular Signal-Regulated MAP KinasesGalectin 1Galectin 3Gene Expression RegulationHumansInflammationInfluenza A virusJanus KinasesBacterial ProteinsCytokinesDEAD Box Protein 58DEAD-box RNA HelicasesExtracellular Signal-Regulated MAP KinasesGalectin 1Galectin 3Janus KinasesLGALS1 protein, humanNeuraminidaseProto-Oncogene Proteins c-aktReceptors, ImmunologicRecombinant ProteinsRIGI protein, humanSOCS1 protein, humanSTAT1 protein, humanSTAT1 Transcription FactorSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsChemokinesCytokinesGalectinNeuraminidaseRIG1Signaling pathwaySOCS

Identifiers

PMID26355912
PMCPMC4624043
OpenAlexW1424462706

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.