Sensory neuron and substance P involvement in symptoms of a zymosan-induced rat model of acute bowel inflammation

Landau, Anne M.; Yashpal, Kiran; Cahill, Caitlin; Louis, Manon St.; Ribeiro‐da‐Silva, Alfredo; Henry, James L.

doi:10.1016/j.neuroscience.2006.11.066

Cited by 12 publications

(12 citation statements)

References 49 publications

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“…Treatment with the NK 1 antagonist SR140333B reduced the febrile response induced by zymosan, suggesting that this neuropeptide participates in this response. In models of acute visceral inflammation and nociception induced by zymosan, the internalization of NK 1 receptors has been observed in neurons in lamina I and sympathetic preganglionic neurons, indicating that the release of substance P and activation of NK 1 receptors are induced by this stimulus [39,40]. These results support the hypothesis that zymosan induces substance P release from neurons.…”

Section: Discussionsupporting

confidence: 73%

Central mediators of the zymosan-induced febrile response

Bastos-Pereira

Fraga

Dreifuss

et al. 2017

Journal of Basic and Clinical Physiology and Pharmacology

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Background: Zymosan is a fungal cell wall protein-carbohydrate complex that is known to activate inflammatory pathways through the Toll-like receptors and is commonly used to induce fever. Nevertheless, the central mediators that are involved in the zymosan-induced febrile response are only partially known. Methods:The present study evaluated the participation of prostaglandins, substance P, endothelin-1 (ET-1), and endogenous opioids (eOPs) in the zymosan-induced febrile response by using inhibitors and antagonists in male Wistar rats. Results: Both nonselective (indomethacin) and selective (celecoxib) cyclooxygenase inhibitors reduced the febrile response induced by an intraperitoneal (i.p.) injection of zymosan. Indomethacin also blocked the increase in the prostaglandin E 2 levels in the cerebrospinal fluid. An intracerebroventricular injection of the neurokinin-1, ET B , and μ-opioid receptor antagonists also reduced the febrile response induced by the i.p. injected zymosan. Moreover, the μ-opioid receptor antagonist CTAP also reduced the febrile response induced by intra-articular injection of zymosan.Conclusions: These results demonstrate that prostaglandins, substance P, ET-1, and eOPs are central mediators of the zymosan-induced febrile response.

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Section: Discussionsupporting

confidence: 73%

Central mediators of the zymosan-induced febrile response

Bastos-Pereira

Fraga

Dreifuss

et al. 2017

Journal of Basic and Clinical Physiology and Pharmacology

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“…In fact, daily administration of the NK2 receptor antagonist SR 48968 also reduces colonic inflammation following TNBS (Mazelin et al, 1998). Since the activation of TRPV1 receptors contributes to the inflammatory cascade, pre-emptive dosing of JYL1421 in the current study likely prevented activation and up-regulation of TRPV1 and the subsequent neurogenic inflammation (Landau et al, 2007).…”

mentioning

confidence: 67%

The role of transient receptor potential vanilloid 1 in mechanical and chemical visceral hyperalgesia following experimental colitis

et al. 2007

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The transient receptor potential vanilloid 1 receptor (TRPV1) is an important nociceptor involved in neurogenic inflammation. We aimed to examine the role of TRPV1 in experimental colitis and in the development of visceral hypersensitivity to mechanical and chemical stimulation. Male Sprague-Dawley rats received a single dose of trinitrobenzenesulfonic acid (TNBS) in the distal colon. In the preemptive group, rats received the TRPV1 receptor antagonist JYL1421 (10 mumol/kg, i.v.) or vehicle 15 min prior to TNBS followed by daily doses for 7 days. In the post-inflammation group, rats received JYL1421 daily for 7 days starting on day 7 following TNBS. The visceromotor response (VMR) to colorectal distension (CRD), intraluminal capsaicin, capsaicin vehicle (pH 6.7) or acidic saline (pH 5.0) was assessed in all groups and compared with controls and naïve rats. Colon inflammation was evaluated with H&E staining and myeloperoxidase (MPO) activity. TRPV1 immunoreactivity was assessed in the thoraco-lumbar (TL) and lumbo-sacral (LS) dorsal root ganglia (DRG) neurons. In the preemptive vehicle group, TNBS resulted in a significant increase in the VMR to CRD, intraluminal capsaicin and acidic saline compared the JYL1421-treated group (P<0.05). Absence of microscopic colitis and significantly reduced MPO activity was also evident compared with vehicle-treated rats (P<0.05). TRPV1 immunoreactivity in the TL (69.1+/-4.6%) and LS (66.4+/-4.2%) DRG in vehicle-treated rats was increased following TNBS but significantly lower in the preemptive JYL1421-treated group (28.6+/-3.9 and 32.3+/-2.3 respectively, P<0.05). JYL1421 in the post-inflammation group improved microscopic colitis and significantly decreased the VMR to CRD compared with vehicle (P<0.05, >/=30 mm Hg) but had no effect on the VMR to chemical stimulation. TRPV1 immunoreactivity in the TL and LS DRG was no different from vehicle or naïve controls. These results suggest an important role for TRPV1 channel in the development of inflammation and subsequent mechanical and chemical visceral hyperalgesia.

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“…CP‐96,345 – the first NK 1 receptor antagonist, discovered in 1991 – proved to be effective in several inflammatory conditions. In cerulein‐induced pancreatitis of the rat, it was able to inhibit the pancreatic plasma extravasation and serum amylase increase ; in the zymosan‐induced acute colitis of the rat, it decreased plasma extravasation ; while in murine experimental autoimmune encephalomyelitis (EAE), it could reduce the clinical and histological signs by stabilization of the blood–brain barrier and suppression of T‐helper 1 immunity .…”

Section: Pro‐inflammatory Neuropeptidesmentioning

confidence: 99%

Neuropeptide receptors as potential drug targets in the treatment of inflammatory conditions

Pintér

Pozsgai

Hajna

et al. 2013

Brit J Clinical Pharma

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Cross-talk between the nervous, endocrine and immune systems exists via regulator molecules, such as neuropeptides, hormones and cytokines. A number of neuropeptides have been implicated in the genesis of inflammation, such as tachykinins and calcitonin gene-related peptide. Development of their receptor antagonists could be a promising approach to anti-inflammatory pharmacotherapy. Anti-inflammatory neuropeptides, such as vasoactive intestinal peptide, pituitary adenylate cyclase-activating polypeptide, a-melanocyte-stimulating hormone, urocortin, adrenomedullin, somatostatin, cortistatin, ghrelin, galanin and opioid peptides, are also released and act on their own receptors on the neurons as well as on different inflammatory and immune cells. The aim of the present review is to summarize the most prominent data of preclinical animal studies concerning the main pharmacological effects of ligands acting on the neuropeptide receptors. Promising therapeutic impacts of these compounds as potential candidates for the development of novel types of anti-inflammatory drugs are also discussed.

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Sensory neuron and substance P involvement in symptoms of a zymosan-induced rat model of acute bowel inflammation

Cited by 12 publications

References 49 publications

Central mediators of the zymosan-induced febrile response

Central mediators of the zymosan-induced febrile response

The role of transient receptor potential vanilloid 1 in mechanical and chemical visceral hyperalgesia following experimental colitis

Neuropeptide receptors as potential drug targets in the treatment of inflammatory conditions

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