ArticleJournal of neuroinflammation2016
TLR2 and TLR9 modulate enteric nervous system inflammatory responses to lipopolysaccharide.
Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 69 citations in OpenAlex.
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- Dual Targeting of TLR9 and cGAS-STING Pathways Attenuates Astrocyte Inflammatory Activation: Potential Implication in Multiple Sclerosis.Neurochemical research · 2025Article
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- Do Bacterial Outer Membrane Vesicles Contribute to Chronic Inflammation in Parkinson's Disease?Journal of Parkinson's disease · 2024Review
- Microbial sensing in the intestine.Protein & cell · 2023Review
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- Gut Dysbiosis and Blood-Brain Barrier Alteration in Hepatic Encephalopathy: From Gut to Brain.Biomedicines · 2023Review
- Gut-brain axis: Mechanisms and potential therapeutic strategies for ischemic stroke through immune functions.Frontiers in neuroscience · 2023Review
- Oxidative Stress-Induced HMGB1 Translocation in Myenteric Neurons Contributes to Neuropathy in Colitis.Biomolecules · 2022Article
- Neonatal development of intestinal neuroimmune interactions.Trends in neurosciences · 2022Review
- The Role of Inflammatory Mediators in the Development of Gastrointestinal Motility Disorders.International journal of molecular sciences · 2022Review
- Neuroimmune Interaction: A Widespread Mutual Regulation and the Weapons for Barrier Organs.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAccumulating evidence suggest that the enteric nervous system (ENS) plays important roles in gastrointestinal inflammatory responses, which could be in part mediated by Toll-like receptor (TLR) activation. The aim of this study was to characterise the expression and functionality of TLR2/4/9 in the ENS.
methodsTLR2/4/9 expression was assessed in the plexuses of adult rats and embryonic ENS cultures by immunofluorescence and quantitative PCR. Following stimulation with TLR2/4/9 ligands or their combinations, activation of NF-kB, production of TNF-α, IL-6 and MCP-1 and chemoattraction of RAW264.7 macrophages were evaluated by means of Western blot, ELISA, immunofluorescence and migration assays in transwell inserts.
resultsTLR2/4/9 staining colocalised with enteric neuronal markers, whereas their presence in enteroglial processes was low to inexistent. Stimulation of ENS cultures with selective ligands induced NF-kB activation and release of cytokines and chemokines by neurons and resident immunocytes. TLR2 neutralisation before lipopolysaccharide (LPS) challenge reduced production of inflammatory mediators, whereas combination of TLR2/4 ligands promoted macrophage migration. Combined stimulation of cultures with LPS and the CpG oligonucleotide 1826 (TLR4/9 ligands) caused a synergic increase in chemoattraction and cytokine production.
conclusionsOur results suggest that the ENS, and particularly enteric neurons, can integrate a variety of microbial signals and respond in a relatively selective fashion, depending on the particular TLRs stimulated. These findings additionally suggest that the ENS is capable of initiating a defensive response against pathogens and expanding inflammation.
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