Immunomodulatory effect of ghrelin in the intestinal mucosa

Eissa, Nour; Ghia, Jean–Eric

doi:10.1111/nmo.12703

Cited by 37 publications

(28 citation statements)

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“…There are some early studies showing that ghrelin increases proliferation and invasiveness of pancreatic adenocarcinoma [ 47 ], hepatoma [ 48 ], and adrenocortical tumor cells [ 49 ]. On the other hand, numerous recent clinical and experimental studies [ 8 , 50 , 51 ], including our present data, indicate that ghrelin exhibits anti-inflammatory effect and plays a role in protecting against cancer-related inflammation [ 52 ] and inflammation-associated carcinogenesis [ 53 ]. For this reason, clinical observations also indicate that low levels of ghrelin are associated with an increased risk of esophageal, gastric, and esophagogastric junctional adenocarcinoma [ 54 , 55 ].…”

Section: Discussionsupporting

confidence: 54%

The Influence of Ghrelin on the Development of Dextran Sodium Sulfate-Induced Colitis in Rats

Matuszyk

Ceranowicz

Warzecha

et al. 2015

BioMed Research International

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Ghrelin has protective and therapeutic effects in the gut. The aim of present studies was to investigate the effect of treatment with ghrelin on the development of colitis evoked by dextran sodium sulfate (DSS). Methods. Studies have been performed on rats. Colitis was induced by adding 5% DSS to the drinking water for 5 days. During this period animals were treated intraperitoneally twice a day with saline or ghrelin given at the dose of 8 nmol/kg/dose. On the sixth day, animals were anesthetized and the severity of colitis was assessed. Results. Treatment with ghrelin during administration of DSS reduced the development of colitis. Morphological features of colonic mucosa exhibited a reduction in the area and deep of mucosal damage. Ghrelin reversed the colitis-induced decrease in blood flow, DNA synthesis, and superoxide dismutase activity in colonic mucosa. These effects were accompanied by a decrease in the colitis-evoked increase in mucosal concentration of interleukin-1β and malondialdehyde. Treatment with ghrelin reversed the DSS-induced reduction in body weight gain. Conclusions. Administration of ghrelin exhibits the preventive effect against the development of DSS-induced colitis. This effect seems to be related to ghrelin's anti-inflammatory and antioxidative properties.

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Section: Discussionsupporting

confidence: 54%

The Influence of Ghrelin on the Development of Dextran Sodium Sulfate-Induced Colitis in Rats

Matuszyk

Ceranowicz

Warzecha

et al. 2015

BioMed Research International

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“…Ghrelin: The circulating levels of ghrelin are elevated in patients with IBD with active inflammation[ 266 , 267 ]. Moreover, circulating ghrelin levels in UC and CD patients are correlated with TNFα, C-reactive protein, the erythrocyte sedimentation rate, and fibrinogen, and negatively correlated with nutritional status parameters[ 42 , 228 , 268 , 269 ].…”

Section: Nes Nepa In Ibdmentioning

confidence: 99%

Gastrointestinal neuroendocrine peptides/amines in inflammatory bowel disease

El‐Salhy

Tefera

Hausken

et al. 2017

WJG

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Inflammatory bowel disease (IBD) is a chronic recurrent condition whose etiology is unknown, and it includes ulcerative colitis, Crohn’s disease, and microscopic colitis. These three diseases differ in clinical manifestations, courses, and prognoses. IBD reduces the patients’ quality of life and is an economic burden to both the patients and society. Interactions between the gastrointestinal (GI) neuroendocrine peptides/amines (NEPA) and the immune system are believed to play an important role in the pathophysiology of IBD. Moreover, the interaction between GI NEPA and intestinal microbiota appears to play also a pivotal role in the pathophysiology of IBD. This review summarizes the available data on GI NEPA in IBD, and speculates on their possible role in the pathophysiology and the potential use of this information when developing treatments. GI NEPA serotonin, the neuropeptide Y family, and substance P are proinflammatory, while the chromogranin/secretogranin family, vasoactive intestinal peptide, somatostatin, and ghrelin are anti-inflammatory. Several innate and adaptive immune cells express these NEPA and/or have receptors to them. The GI NEPA are affected in patients with IBD and in animal models of human IBD. The GI NEPA are potentially useful for the diagnosis and follow-up of the activity of IBD, and are candidate targets for treatments of this disease.

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“…Recently, the anti‐IL‐12p40 monoclonal antibody ( Ustekinumab ™) has demonstrated good clinical efficacy in a group of UC patients resistant to anti‐TNF therapy (Sandborn et al, ) demonstrating that blocking the communication between CD11c + and T‐cells can result in a decrease in the activity of the IL‐12/23 pro‐inflammatory pathway (Fitzpatrick, ). Among various intracellular pathways that activate CD11c + cell functions, NF‐κB pathway regulates IL‐12/23 production (Kaiko et al, ; Rescigno, Martino, Sutherland, Gold, & Ricciardi‐Castagnoli, ; Tas et al, ), and in active UC, activation of NF‐κB is increased in lamina propria mononuclear cells; therefore, inhibition of the NF‐κB pathway has been proposed as a therapeutic strategy (Eissa, Hussein, Kermarrec, Elgazzar, et al, ; Eissa & Ghia, ; Eissa, Hussein, Hendy, Bernstein, & Ghia, ).…”

Section: Introductionmentioning

confidence: 99%

Semaphorin‐3E attenuates intestinal inflammation through the regulation of the communication between splenic CD11C⁺ and CD4⁺CD25⁻ T‐cells

Kermarrec

Eissa

Wang

et al. 2019

British J Pharmacology

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Background and Purpose: An alteration in the communication between the innate and adaptive immune cells is a hallmark of ulcerative colitis (UC). Semaphorin-3E (SEMA3E), a secreted guidance protein, regulates various immune responses. Experimental Approach: We investigated the expression of SEMA3E in colonic biopsies of active UC patients and its mechanisms in Sema3e −/− mice using an experimental model of UC.Key Results: SEMA3E level was decreased in active UC patients and negatively correlated with pro-inflammatory mediators. Colonic expression of SEMA3E was reduced in colitic Sema3e +/+ mice, and recombinant (rec-) Plexin-D1 treatment exacerbated disease severity. In vivo rec-SEMA3E treatment restored SEMA3E level in colitic Sema3e +/+ mice. In Sema3e −/− mice, disease severity was increased, and rec-SEMA3E ameliorated these effects. Lack of Sema3e increased the expression of CD11c and CD86 markers. Colitic Sema3e −/− splenocytes and splenic CD11c + cells produced more IL-12/23 and IFN-γ compared to Sema3e +/+ , and rec-SEMA3E reduced their release as much as NF-κB inhibitors, whereas an NF-κB activator increased their production and attenuated the effect of rec-SEMA3E. Colitic Sema3e −/− splenic CD11c + /CD4 + CD25 − T-cell co-cultures produced higher concentrations of IFN-γ and IL-17 when compared to colitic Sema3e +/+ splenic cell co-cultures, and rec-SEMA3E decreased these effects. In vitro, anti-IL-12p19 and -12p35 antibodies and rec-IL-12 and -23 treatment confirmed the crosstalk between CD11c + and CD4 + CD25 − T-cells.Conclusion and Implications: SEMA3E is reduced in colitis and modulates colonic inflammation by regulating the interaction between CD11c + and CD4 + CD25 − T-cells via an NF-κB-dependent mechanism. Thus, SEMA3E could be a potential therapeutic target for UC patients.

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Immunomodulatory effect of ghrelin in the intestinal mucosa

Cited by 37 publications

References 50 publications

The Influence of Ghrelin on the Development of Dextran Sodium Sulfate-Induced Colitis in Rats

The Influence of Ghrelin on the Development of Dextran Sodium Sulfate-Induced Colitis in Rats

Gastrointestinal neuroendocrine peptides/amines in inflammatory bowel disease

Semaphorin‐3E attenuates intestinal inflammation through the regulation of the communication between splenic CD11C⁺ and CD4⁺CD25⁻ T‐cells

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Immunomodulatory effect of ghrelin in the intestinal mucosa

Cited by 37 publications

References 50 publications

The Influence of Ghrelin on the Development of Dextran Sodium Sulfate-Induced Colitis in Rats

The Influence of Ghrelin on the Development of Dextran Sodium Sulfate-Induced Colitis in Rats

Gastrointestinal neuroendocrine peptides/amines in inflammatory bowel disease

Semaphorin‐3E attenuates intestinal inflammation through the regulation of the communication between splenic CD11C+ and CD4+CD25− T‐cells

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Semaphorin‐3E attenuates intestinal inflammation through the regulation of the communication between splenic CD11C⁺ and CD4⁺CD25⁻ T‐cells