ArticleFrontiers in veterinary science2014
Critical Role of Glycogen Synthase Kinase-3β in Regulating the Avian Heterophil Response to Salmonella enterica Serovar Enteritidis.
Article in Frontiers in veterinary science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Methods and approaches to disease mechanisms using systems kinomics.Synthetic and systems biotechnology · 2018Review
- Immunometabolism and the Kinome Peptide Array: A New Perspective and Tool for the Study of Gut Health.Frontiers in veterinary science · 2015Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A microarray-assisted gene expression screen of chicken heterophils revealed glycogen synthase kinase-3β (GSK-3β), a multifunctional Ser/Thr kinase, to be consistently upregulated 30-180 min following stimulation with Salmonella enterica serovar Enteritidis (S. Enteritidis). The present study was designed to delineate the role of GSK-3β in regulating the innate function of chicken heterophils in response to S. Enteritidis exposure. Using a specific GSK-3β ELISA assay, 30 min after infection with S. Enteritidis, heterophils had a significant decrease (p ≤ 0.05) in total GSK-3β, but a significant increase (p ≤ 0.05) in phosphorylated GSK-3β (Ser9). By 60 min post-infection, there was no difference in the amount of phosphorylated GSK-3β (Ser9) in either the uninfected and infected heterophils. S. Enteritidis interaction with heterophils alters GSK-3β activity by stimulating phosphorylation at Ser9 and that peaks by 30 min post-infection. Further, inhibition of GSK3β with lithium chloride resulted in a significant decrease (p ≤ 0.05) in NF-κB activation and expression of IL-6, but induces a significant increase (p ≤ 0.05) in the expression of the anti-inflammatory cytokine, IL-10. Using a phospho-specific antibody array confirmed the phosphorylation of GSK-3β (Ser9) as well as the phosphorylation of the downstream cytokine-activated intracellular signaling pathway involved in stimulating immune responses, IκB, the IκB subunit IKK-β, and the NF-κB subunits p105, p65, and c-Rel. Our data revealed that the phosphorylation of GSK-3β (Ser9) is responsible for inducing and controlling an innate response to the bacteria. Our findings suggest that the repression of GSK-3 activity is beneficial to the host cell and may act as a target for treatment in controlling intestinal colonization in chickens. Further experiments will define the in vivo modulation of GSK-3 as a potential alternative to antibiotics in salmonella and other intestinal bacterial infections.
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Registered trials
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.