ArticleReceptors for sensory neuropeptides in human inflammatory diseases: Implications for the effector role of sensory neurons☆
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Cited by (121)
Mechanisms and Consequences of Intestinal Inflammation
2012, Physiology of the Gastrointestinal Tract, Two Volume SetMechanisms and Consequences of Intestinal Inflammation
2012, Physiology of the Gastrointestinal TractOpposite effects of substance P and calcitonin gene-related peptide in oxazolone colitis
2012, Digestive and Liver DiseaseCitation Excerpt :Their pathogenesis has been poorly understood, but there is increasing evidence that a pathological neuroimmune interaction is responsible for both diseases [1]. Neuropeptides such as calcitonin gene-related peptide (CGRP) and substance P (SP) that are released from depolarized peptidergic sensory neurons appear to play a crucial role in both human and experimental colitis [2–15]. Biopsy specimens of inflamed regions from patients with CD and UC demonstrate increased SP-positive nerve fibre density, SP content, and SP receptor binding compared to controls [9–15].
Characterization of Autonomic Nerve Markers and Lymphocyte Subsets in the Ileal Peyer's Patch of Pigs Infected Experimentally with Brachyspira hyodysenteriae
2010, Journal of Comparative PathologyCitation Excerpt :The increased tissue concentration of SP (by about one-third of the normal value) in the dysenteric pigs suggests that this substance may also play a role in regulation of the porcine Peyer’s patch in both physiological and pathological states. In the light of the present results, the findings of Mantyh et al. (1989) describing the location and concentration of receptor binding sites for sensory neurotransmitters in the colon in two human inflammatory diseases, ulcerative colitis and Crohn’s disease, are of note. Those authors found that of the nine receptor binding sites examined, only the SP binding sites associated with lymphoid aggregates, arterioles and venules were significantly up-regulated in the inflamed tissue.
Tachykinins and Neurogenic Inflammation at Visceral Level
2009, NeuroImmune BiologyCitation Excerpt :However, in chronic inflammatory bowel diseases, tachykinin NK1 receptors have been found markedly upregulated, compared to their density measured in the intestine of normal subjects. Upregulation involves either sites where NK1 receptors are normally present (e.g., vasculature, epithelial cells), or even sites where they are normally absent (ectopic expression: e.g., in intestinal lymphoid aggregates) [197,232]. Recently, Renzi and coworkers [233] have shown that, in addition to NK1, also NK2 receptor expression is markedly increased on inflammatory cells (eosinophils) of the lamina propria of patients with Crohn’s disease or ulcerative colitis, suggesting their possible involvement in the above pathologies.
Distribution and Chemical Coding of Intramural Neurons in the Porcine Ileum During Proliferative Enteropathy
2008, Journal of Comparative Pathology
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This work supported by the Southern California Arthritis Foundation, Sloan Foundation and NS-23970, NS-22961, DK-40260.