ArticlePloS one2014
Mycobacteria bypass mucosal NF-kB signalling to induce an epithelial anti-inflammatory IL-22 and IL-10 response.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 38 citations in OpenAlex.
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- Lung epithelial cells interact with immune cells and bacteria to shape the microenvironment in tuberculosis.Thorax · 2022Review
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- Adjuvanting Allergen Extracts for Sublingual Immunotherapy: Calcitriol Downregulates CXCL8 Production in Primary Sublingual Epithelial Cells.Frontiers in immunology · 2020Article
- Target the Host, Kill the Bug; Targeting Host Respiratory Immunosuppressive Responses as a Novel Strategy to Improve Bacterial Clearance During Lung Infection.Frontiers in immunology · 2020Review
- The humoral immune response is essential for successful vaccine protection against paratuberculosis in sheep.BMC veterinary research · 2019Article
- GSK3β inhibition attenuates LPS-induced IL-6 expression in porcine adipocytes.Scientific reports · 2018Article
- Identification of genes associated with susceptibility to Mycobacterium avium ssp. paratuberculosis (Map) tissue infection in Holstein cattle using gene set enrichment analysis-SNP.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Article
- Targeting CREB-binding protein overrides LPS induced radioresistance in non-small cell lung cancer cell lines.Oncotarget · 2018Article
- The crucial roles of Th17-related cytokines/signal pathways in M. tuberculosis infection.Cellular & molecular immunology · 2018Review
- Epithelial Cells Attenuate Toll-Like Receptor-Mediated Inflammatory Responses in Monocyte-Derived Macrophage-Like Cells toMediators of inflammation · 2018Article
- ArfGAP1 restrictsEMBO reports · 2018Article
- Divergent Functions of TLR2 on Hematopoietic and Nonhematopoietic Cells during Chronic Mycobacterium tuberculosis Infection.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Mycobacteria Manipulate G-Protein-Coupled Receptors to Increase Mucosal Rac1 Expression in the Lungs.Journal of innate immunity · 2017Article
- Pilot study of lithium to restore intestinal barrier function in severe graft-versus-host disease.PloS one · 2017Observational
- Development of a non-infectious rat model of acute exacerbation of idiopathic pulmonary fibrosis.Journal of thoracic disease · 2017Article
- Downregulation of vimentin in macrophages infected with live Mycobacterium tuberculosis is mediated by Reactive Oxygen Species.Scientific reports · 2016Article
- Interleukin-10 Family and Tuberculosis: An Old Story Renewed.International journal of biological sciences · 2016Review
- Adjunct Strategies for Tuberculosis Vaccines: Modulating Key Immune Cell Regulatory Mechanisms to Potentiate Vaccination.Frontiers in immunology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms by which mycobacteria subvert the inflammatory defence to establish chronic infection remain an unresolved question in the pathogenesis of tuberculosis. Using primary epithelial cells, we have analysed mycobacteria induced epithelial signalling pathways from activation of TLRs to cytokine secretion. Mycobacterium bovis bacilli Calmette-Guerin induced phosphorylation of glycogen synthase kinase (GSK)3 by PI3K-Akt in the signalling pathway downstream of TLR2 and TLR4. Mycobacteria did not suppress NF-κB by activating the peroxisome proliferator-activated receptor γ. Instead the pro-inflammatory NF-κB was bypassed by mycobacteria induced GSK3 inhibition that promoted the anti-inflammatory transcription factor CREB. Mycobacterial infection did not thus induce mucosal pro-inflammatory response as measured by TNFα and IFNγ secretion, but led to an anti-inflammatory IL-10 and IL-22 production. Apart from CREB, MAP3Ks p38 and ERK1/2 activated the transcription factor AP-1 leading to IL-6 production. Interestingly, blocking of TLR4 before infection decreased epithelial IL-6 secretion, but increased the CREB-activated IL-10 production. Our data indicate that mycobacteria suppress epithelial pro-inflammatory production by suppressing NF-κB activation thereby shifting the infection towards an anti-inflammatory state. This balance between the host immune response and the pathogen could determine the outcome of infection.
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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.