Neuroimmune Interactions in Experimental Colitis

Fehér, Erzsébet; Altdorfer, Károly; Bagaméri, Gábor; Fehér, János

doi:10.1159/000054287

Cited by 27 publications

(16 citation statements)

References 23 publications

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“…The activated lymphocytes produce lymphokines and inflammatory mediators. Evidence for bidirectional communication between nervous and immune systems is well established in the alimentary tract [11,18,35,36]. Changes in immune function might influence the distribution of nerves and the expression of neural transmitter receptors in immunocytes [37].…”

Section: Discussionmentioning

confidence: 99%

Neuroimmune Link in the Mucosa of Chronic Gastritis with Helicobacter pylori Infection

et al. 2006

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It is suggested that different neuropeptides regulate gastric mucosal integrity and participate in the development of chronic gastritis. The aim of this study was to examine the roles and changes of immunoreactive (IR) nerves and immunocompetent cells in human gastritis. Immunohistochemical, immunocytochemical, and confocal laser microscopic methods were used. All investigated nerve fibers were found in different quantities in the mucosa of both control and gastritis samples. The number of SP, NPY, and VIP IR nerve fibers increased significantly (P < 0.05) in gastritis. No IR immunocompetent cells (lymphocytes, plasma cells, mast cells) were found in the control, however, some showed NPY (16.8%) and SP (9.4%) immunoreactivity in chronic gastritis. The distance between nerve fibers and immunocompetent cells was 200 nm to 1 microm. In conclusion, the increased number of SP, NPY, and VIP IR nerves and IR immunocytes suggests that they participate in development of neurogenic inflammation, repairing processes of chronic gastritis.

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Section: Discussionmentioning

confidence: 99%

Neuroimmune Link in the Mucosa of Chronic Gastritis with Helicobacter pylori Infection

et al. 2006

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“…VIP nerve fibers can be traced to the tip of the villus, with frequent interactions with immunocompetent cells; the density of VIPimmune cell interaction increases in models of acute inflammation (15) and may act to reset the secretory and motor activity of the gut in a protective fashion.…”

Section: Effects Of Glp-2 On Intestinal Morphology Crypt Proliferamentioning

confidence: 99%

Enteric neural pathways mediate the anti-inflammatory actions of glucagon-like peptide 2

Sigalet¹,

Wallace²,

Holst³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

158

149

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is an important regulator of nutritional absorptive capacity with antiinflammatory actions. We hypothesized that GLP-2 reduces intestinal mucosal inflammation by activation of vasoactive intestinal polypeptide (VIP) neurons of the submucosal plexus. Ileitis or colitis was induced in rats by injection of trinitrobenzene sulfonic acid (TNBS), or colitis was induced by administration of dextran sodium sulfate (DSS) in drinking water. Subsets of animals received (1-33)-GLP-2 (50 g/kg sc bid) either immediately or 2 days after the establishment of inflammation and were followed for 3-5 days. The involvement of VIP neurons was assessed by concomitant administration of GLP-2 and the VIP antagonist [Lys 1 -Pro 2,5 -Arg 3,4 -Tyr 6 ]VIP and by immunohistochemical labeling of GLP-2-activated neurons. In all models, GLP-2 treatment, whether given immediately or delayed until inflammation was established, resulted in significant improvements in animal weights, mucosal inflammation indices (myeloperoxidase levels, histological mucosal scores), and reduced levels of inflammatory cytokines (IFN-␥, TNF-␣, IL-1␤) and inducible nitric oxide synthase, with increased levels of IL-10 in TNBS ileitis and DSS colitis. Reduced rates of crypt cell proliferation and of apoptosis within crypts in inflamed tissues were also noted with GLP-2 treatment. These effects were abolished with coadministration of GLP-2 and the VIP antagonist. GLP-2 was shown to activate neurons and to increase the number of cells expressing VIP in the submucosal plexus of the ileum. These findings suggest that GLP-2 acts as an anti-inflammatory agent through activation of enteric VIP neurons, independent of proliferative effects. They support further studies to examine the role of neural signaling in the regulation of intestinal inflammation. vasoactive intestinal peptide; trinitrobenzene sulfonic acid colitis; dextran sodium sulfate colitis; Crohn's disease THE ENTEROENDOCRINE HORMONE glucagon-like peptide-2 (GLP-2) is thought to act primarily as a regulator of intestinal nutrient absorption and as an intestinal-specific trophic factor (10, 12, 26). As a trophic factor, GLP-2 stimulates crypt cell proliferation, nutrient transporter expression, and intestinal blood flow (27) through actions on a specific receptor system primarily localized to enteric neurons and enteroendocrine cells (4,20,35). In studies using dextran sodium sulfate (DSS) and indomethacin models of intestinal inflammation, GLP-2 stimulation has been shown to improve mucosal healing (6, 13, 24); mechanistically, this was ascribed to an increased crypt cell proliferation rate (13).Given the evidence that GLP-2 receptors appear to be localized to the enteric nervous system, we speculated that GLP-2 may induce anti-inflammatory effects via this pathway. Specifically, vasoactive intestinal polypeptide (VIP) has been shown to act as an anti-inflammatory agent (2), and so we hypothesized that GLP-2 may act by stimulating neuronal VIP release in the intestinal submucosa and mucosa. Subsequently, it has bee...

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“…Számos immunsejt (lymphocyták és makrofágok) is képes különböző körülmények (gyulladás és sérülés) során neuropeptideket termelni és ugyanazon peptidreceptorokat is expresszálni [16,17]. Az aktivált immunsejtekből felszabadult neuropeptidek visszahathatnak a termelődésük helyére (immunsejt, axon) és fokozhatják az idegrostokból felszabaduló neuropeptidek hatását, így fokozhatják vagy csökkenthetik a gyulladást.…”

Section: Npy Hatása Gyulladásos Folyamatokbanunclassified

Neuropeptid Y és P anyag immunreaktív idegrostok és immunkompetens sejtek változása hepatitisben

Fehér

2015

Orvosi Hetilap

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A neuropeptid Y és a P anyag olyan neuropeptidek, amelyek fontos szerepet játszanak az immunsejtek működésében és a gyulladásos folyamatok fenntartásában és eliminálásában. Hepatitisben mindkét neuropeptidet tartalmazó idegrost mennyisége megnövekszik, a neuropeptid Y immunreaktív rostok növekedése szignifi káns. Számos lymphocytá-ban és hízósejtben szintén neuropeptid Y és a P anyag mutatható ki. Gyakran fi gyelhető meg közeli kapcsolat (kevesebb mint 1 μm) a neuropeptid Y immunreaktív idegrostok és a neuropeptid Y pozitív immunsejtek között. Az immunsejtek egy részében tumornekrózis-faktor-α és nukleáris faktor kappa-B-jelölődés is megfi gyelhető. Néhány P anyagot tartalmazó immunsejtben kolokalizációban fi gyelhető meg a tumornekrózis-faktor-α. Feltételezhető, hogy hepatitisben az idegrostokból és immunsejtekből felszabaduló neuropeptid Y és P anyag részt vesz a gyulladásos folyamatokban és azok eliminálásában. Orv. Hetil., 2015, 156(47), 1892-1897. Kulcsszavak: hepatitis, neuropeptid Y, P anyag, neuroimmun-moduláció Changes in neuropeptide Y and substance P immunoreactive nerve fi bres and immune competent cells in hepatitisNeuropeptide Y and substance P were thought to play a role in the function of immune cells and in amplifi cation or elimination of the infl ammatory processes. In hepatitis the number of both neuropeptide Y and substance P immunoreactive nerve fi bres are increased, where the increase of neoropeptide Y is signifi cant. A large number of lymphocytes and mast cells are also stained for neuropeptide Y and substance P. Very close associations (less than 1 μm) were observed between neuropeptide Y immunoreactive nerve fi bres and immune cells stained also with neuropeptide Y. Some immune cells were also found to be immunoreactive for tumor necrosis factor-α and NF-κB. Some of the SP IR immunocells were also stained for TNF-α and nuclear factor kappaB. Based on these data it is hypothesized that neuropeptid Y and substance P released from nerve fi bres and immune cells play a role in infl ammation and elimination of infl ammation in hepatitis.

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Neuroimmune Interactions in Experimental Colitis

Cited by 27 publications

References 23 publications

Neuroimmune Link in the Mucosa of Chronic Gastritis with Helicobacter pylori Infection

Neuroimmune Link in the Mucosa of Chronic Gastritis with Helicobacter pylori Infection

Enteric neural pathways mediate the anti-inflammatory actions of glucagon-like peptide 2

Neuropeptid Y és P anyag immunreaktív idegrostok és immunkompetens sejtek változása hepatitisben

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