Interleukin 1β-induced increase in substance P in rat myenteric plexus
References (30)
- et al.
Receptors for sensory neuropeptides in human inflammatory diseases: implications for the effector role of sensory neurons
Peptides
(1989) - et al.
Impaired sympathetic nerve function in the inflamed rat intestine
Gastroenterology
(1991) - et al.
Increased levels of substance P in the myenteric plexus of Trichinella-infected rats
Gastroenterology
(1992) - et al.
Peptides in the gastrointestinal tract in human immunodeficiency virus infection
Gastroenterology
(1992) - et al.
Distribution of substance P in the rat gastrointestinal tract—lack of effect of capsaicin pretreatment
Eur J Pharmacol
(1980) - et al.
Projections of peptide-containing neurons in rat small intestine
Neuroscience
(1987) - et al.
Transforming growth factor beta has neurotrophic actions on sensory neurons in vitro and is synergistic with nerve growth factor
Dev Biol
(1992) Neuropeptides and inflammation: the role of substance P
Annu Rev Med
(1989)- et al.
Distribution and quantification of gut neuropeptides in normal intestine and inflammatory bowel diseases
Dig Dis Sci
(1987) - et al.
Peptide-containing nerve fibres in the gut wall in Crohn's disease
Gut
(1983)
Colonic substance P levels are increased in ulcerative colitis and decreased in chronic severe constipation
Dig Dis Sci
Receptor binding sites for substance P, but not substance K or neuromedin K, are expressed in high concentrations by arterioles, venules, and lymph nodules in surgical specimens obtained from patients with ulcerative colitis and Crohn's disease
Impaired acetylcholine release from the myenteric plexus of Trichinella-infected rats
Am J Physiol
Cytokine mRNA profile in smooth muscle from the inflamed intestine of the nematode-infected rat (abstr)
Gastroenterology
Conditioned medium from activated splenocytes increases substance P in sympathetic ganglia
J Neurosci Res
Cited by (51)
The Enteric Network: Interactions between the Immune and Nervous Systems of the Gut
2017, ImmunityCitation Excerpt :The abundance and close proximity of neuronal varicosities to immune cells should make this unsurprising, but it is important in the study of immune responses to consider the effector functions of cytokine molecules on non-immune cell types. For example, IL-1β is heightened in the intestines of patients with inflammatory bowel disease (IBD) (Ligumsky et al., 1990), and in accordance with prior discussions, IL-1β also induces SP production in the ENS (Hurst et al., 1993). Furthermore, IL-1β engagement with its cognate receptor in ex vivo ENS preparations suppresses electric-field stimulation (EFS)-evoked release of ACh and norepinephrine (Collins et al., 1992).
Impact of genetic polymorphisms on the pathogenesis of idiopathic achalasia: Association with IL33 gene variant
2014, Human ImmunologyCitation Excerpt :The influence of cytokines in the changes in neurochemical phenotype of myenteric neurones was observed in an ex vivo model of human healthy gastric fundus incubated with sera from achalasic patients [45]. The changed phenotype of myenteric plexus was explained by the increase in IL-8 levels in the serum of achalasia patients compared with controls, by the ability of cytokines, such as interleukin 1β, to regulate gene expression in enteric neurones [46,47], and by the presence of inflammatory cells in the myenteric plexus in patients with achalasia [48,49]. Interestingly, the contribution of the IL-33/ST2 pathway to the pathogenesis of certain viral infections has been also observed.
Inflammation as a basis for functional GI disorders
2004, Best Practice and Research: Clinical GastroenterologyChronic treatment with interleukin-1β attenuates contractions by decreasing the activities of CPI-17 and MYPT-1 in intestinal smooth muscle
2003, Journal of Biological ChemistryExpression of neuropeptides and cytokines at the extensor carpi radialis brevis muscle origin
2002, Journal of Shoulder and Elbow SurgeryCitation Excerpt :In the cardiovascular system, CGRP has the potential to inhibit the proliferation of vascular smooth muscle cells (VSMCs), serving to counterbalance the stimulatory effects of IL-1 on VSMC proliferation.23 Interleukin 1β (IL-1β) increased immunoreactive substance P in the longitudinal muscle–myentric plexus of the inflamed intestine of Trichinella spinalis–infected rats.20 Thus, the interaction between neuropeptide and cytokines is considered to be important in clarifying the mechanism governing pathologic states.
Immune-mediated neural dysfunction in a murine model of chronic Helicobacter pylori infection
2002, GastroenterologyCitation Excerpt :SP and CGRP are the main sensory and proinflammatory neurotransmitters in the gut. Increase in SP content in gut has been reported during T. spiralis infection48 as well as after incubating the intestinal tissue with interleukin 1β,49 a cytokine produced by several MN cell types. We have observed a 2.5- and 2-fold increase in the density of SP- and CGRP-IR nerves, respectively, both in the gastric wall and dorsal horn of the spinal cord of infected animals.