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Intraluminal acid activates esophageal nodose C fibers after mast cell activation.
Am J Physiol Gastrointest Liver Physiol. 2014 Feb; 306(3):G200-7.AJ

Abstract

Acid reflux in the esophagus can induce esophageal painful sensations such as heartburn and noncardiac chest pain. The mechanisms underlying acid-induced esophageal nociception are not clearly understood. In our previous studies, we characterized esophageal vagal nociceptive afferents and defined their responses to noxious mechanical and chemical stimulation. In the present study, we aim to determine their responses to intraluminal acid infusion. Extracellular single-unit recordings were performed in nodose ganglion neurons with intact nerve endings in the esophagus using ex vivo esophageal-vagal preparations. Action potentials evoked by esophageal intraluminal acid perfusion were compared in naive and ovalbumin (OVA)-challenged animals, followed by measurements of transepithelial electrical resistance (TEER) and the expression of tight junction proteins (zona occludens-1 and occludin). In naive guinea pigs, intraluminal infusion with either acid (pH = 2-3) or capsaicin did not evoke an action potential discharge in esophageal nodose C fibers. In OVA-sensitized animals, following esophageal mast cell activation by in vivo OVA inhalation, intraluminal acid infusion for about 20 min started to evoke action potential discharges. This effect is further confirmed by selective mast cell activation using in vitro tissue OVA challenge in esophageal-vagal preparations. OVA inhalation leads to decreased TEER and zona occludens-1 expression, suggesting an impaired esophageal epithelial barrier function after mast cell activation. These data for the first time provide direct evidence of intraluminal acid-induced activation of esophageal nociceptive C fibers and suggest that mast cell activation may make esophageal epithelium more permeable to acid, which subsequently may increase esophageal vagal nociceptive C fiber activation.

Authors+Show Affiliations

Division of Gastroenterology and Hepatology, Department of Medicine, University of Michigan Medical School, Ann Arbor, Michigan; and.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

24264049

Citation

Zhang, Shizhong, et al. "Intraluminal Acid Activates Esophageal Nodose C Fibers After Mast Cell Activation." American Journal of Physiology. Gastrointestinal and Liver Physiology, vol. 306, no. 3, 2014, pp. G200-7.
Zhang S, Liu Z, Heldsinger A, et al. Intraluminal acid activates esophageal nodose C fibers after mast cell activation. Am J Physiol Gastrointest Liver Physiol. 2014;306(3):G200-7.
Zhang, S., Liu, Z., Heldsinger, A., Owyang, C., & Yu, S. (2014). Intraluminal acid activates esophageal nodose C fibers after mast cell activation. American Journal of Physiology. Gastrointestinal and Liver Physiology, 306(3), G200-7. https://doi.org/10.1152/ajpgi.00142.2013
Zhang S, et al. Intraluminal Acid Activates Esophageal Nodose C Fibers After Mast Cell Activation. Am J Physiol Gastrointest Liver Physiol. 2014;306(3):G200-7. PubMed PMID: 24264049.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Intraluminal acid activates esophageal nodose C fibers after mast cell activation. AU - Zhang,Shizhong, AU - Liu,Zhenyu, AU - Heldsinger,Andrea, AU - Owyang,Chung, AU - Yu,Shaoyong, Y1 - 2013/11/21/ PY - 2013/11/23/entrez PY - 2013/11/23/pubmed PY - 2014/3/26/medline KW - C fiber KW - acid KW - esophagus KW - mast cell KW - vagal afferent SP - G200 EP - 7 JF - American journal of physiology. Gastrointestinal and liver physiology JO - Am J Physiol Gastrointest Liver Physiol VL - 306 IS - 3 N2 - Acid reflux in the esophagus can induce esophageal painful sensations such as heartburn and noncardiac chest pain. The mechanisms underlying acid-induced esophageal nociception are not clearly understood. In our previous studies, we characterized esophageal vagal nociceptive afferents and defined their responses to noxious mechanical and chemical stimulation. In the present study, we aim to determine their responses to intraluminal acid infusion. Extracellular single-unit recordings were performed in nodose ganglion neurons with intact nerve endings in the esophagus using ex vivo esophageal-vagal preparations. Action potentials evoked by esophageal intraluminal acid perfusion were compared in naive and ovalbumin (OVA)-challenged animals, followed by measurements of transepithelial electrical resistance (TEER) and the expression of tight junction proteins (zona occludens-1 and occludin). In naive guinea pigs, intraluminal infusion with either acid (pH = 2-3) or capsaicin did not evoke an action potential discharge in esophageal nodose C fibers. In OVA-sensitized animals, following esophageal mast cell activation by in vivo OVA inhalation, intraluminal acid infusion for about 20 min started to evoke action potential discharges. This effect is further confirmed by selective mast cell activation using in vitro tissue OVA challenge in esophageal-vagal preparations. OVA inhalation leads to decreased TEER and zona occludens-1 expression, suggesting an impaired esophageal epithelial barrier function after mast cell activation. These data for the first time provide direct evidence of intraluminal acid-induced activation of esophageal nociceptive C fibers and suggest that mast cell activation may make esophageal epithelium more permeable to acid, which subsequently may increase esophageal vagal nociceptive C fiber activation. SN - 1522-1547 UR - https://www.unboundmedicine.com/medline/citation/24264049/Intraluminal_acid_activates_esophageal_nodose_C_fibers_after_mast_cell_activation_ L2 - https://journals.physiology.org/doi/10.1152/ajpgi.00142.2013?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -