ArticleJournal of neuroimmunology2013
Capsaicin-sensitive vagal afferent neurons contribute to the detection of pathogenic bacterial colonization in the gut.
Article in Journal of neuroimmunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 31 citations in OpenAlex.
- A Comprehensive Review of the Gut-Microbiota-Brain Axis in Alzheimer's Disease: From Pathophysiology to Potential Therapies.Pathogens (Basel, Switzerland) · 2026Review
- Bidirectional regulation of the brain-gut-microbiota axis following traumatic brain injury.Neural regeneration research · 2025Article
- Microfluidic compartmentalization of rat vagal afferent neurons to model gut-brain axis.Bioelectronic medicine · 2024Article
- Butterflies in the gut: the interplay between intestinal microbiota and stress.Journal of biomedical science · 2023Review
- Article
- Neural Immune Communication in the Control of Host-Bacterial Pathogen Interactions in the Gastrointestinal Tract.Infection and immunity · 2020Review
- Glucagon-Like Peptide-1 Secreting L-Cells Coupled to Sensory Nerves Translate Microbial Signals to the Host Rat Nervous System.Frontiers in cellular neuroscience · 2020Article
- Review
- Neural pathways involved in infection-induced inflammation: recent insights and clinical implications.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2018Review
- Sensory neuron regulation of gastrointestinal inflammation and bacterial host defence.Journal of internal medicine · 2017Review
- Visceral Inflammation and Immune Activation Stress the Brain.Frontiers in immunology · 2017Review
- Neuroimmune pharmacological approaches.Current opinion in pharmacology · 2015Review
- Exercise and the microbiota.Gut microbes · 2015Article
- Divergent neuroendocrine responses to localized and systemic inflammation.Seminars in immunology · 2014Review
- Chronic functional bowel syndrome enhances gut-brain axis dysfunction, neuroinflammation, cognitive impairment, and vulnerability to dementia.Neurochemical research · 2014Review
- TLR4 Signaling Selectively and Directly Promotes CGRP Release from Vagal Afferents in the Mouse.eNeuroArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Vagal activation can reduce inflammation and disease activity in various animal models of intestinal inflammation via the cholinergic anti-inflammatory pathway. In the current model of this pathway, activation of descending vagal efferents is dependent on a signal initiated by stimulation of vagal afferents. However, little is known about how vagal afferents are activated, especially in the context of subclinical or clinical pathogenic bacterial infection. To address this question, we first determined if selective lesions of capsaicin-sensitive vagal afferents altered c-Fos expression in the nucleus of the solitary tract (nTS) after mice were inoculated with either Campylobacter jejuni or Salmonella typhimurium. Our results demonstrate that the activation of nTS neurons by intraluminal pathogenic bacteria is dependent on intact, capsaicin sensitive vagal afferents. We next determined if inflammatory mediators could cause the observed increase in c-Fos expression in the nTS by a direct action on vagal afferents. This was tested by the use of single-cell calcium measurements in cultured vagal afferent neurons. We found that tumor necrosis factor alpha (TNFα) and lipopolysaccharide (LPS) directly activate cultured vagal afferent neurons and that almost all TNFα and LPS responsive neurons were sensitive to capsaicin. We conclude that activation of the afferent arm of the parasympathetic neuroimmune reflex by pathogenic bacteria in the gut is dependent on capsaicin sensitive vagal afferent neurons and that the release of inflammatory mediators into intestinal tissue can be directly sensed by these neurons.
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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.