Ghrelin receptor modulates T helper cells during intestinal inflammation

Giovangiulio, Martina Di; Stakenborg, Nathalie; Bosmans, Goele; Meroni, Elisa; Farro, Giovanna; Gomez‐Pinilla, Pedro J.; Depoortere, Inge; Boeckxstaens, Guy E.; Matteoli, Gianluca

doi:10.1111/nmo.12640

Cited by 5 publications

(9 citation statements)

References 43 publications

(66 reference statements)

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“…From these studies, the possible interpretation of ghrelin's effects is linked to inhibition of monocytes/macrophages and Th1 responses, which is associated with increased IL‐10 and TGF β production via direct action on the lamina propria mononuclear (LPMC) and draining mesenteric lymph nodes (MLN) cells. Another study using a DSS model in rats showed that exogenous ghrelin administration improved the disease activity via decreased immune cell infiltration, reduced pro‐inflammatory mediators associated with a suppression of the Th1‐mediated responses and increased anti‐inflammatory cytokines, supporting the findings of Di Giovangiulio et al . demonstrating that ghrelin mediates T‐cell response.…”

Section: Ghrelin and Mechanistic Considerationssupporting

confidence: 53%

“…Ghrelin and its receptor are expressed in T‐helper immune cells. Intestinal inflammation was studied by Di Giovangiulio et al . using the T‐cell transfer model of chronic colitis in recombination activating gene 1 knockout (Rag1 −/− ) mice by adoptive transfer of CD4 Th cells from ghrelin receptor knockout (GRLN‐R −/− ) and wild type mice; their results highlighted the protective effect of ghrelin in chronic colitis.…”

Section: Ghrelin and Mechanistic Considerationsmentioning

confidence: 99%

“…mTOR negatively regulates the NF‐ κ B pathway, which can explain the dual cytokine modulatory effect induced by ghrelin, through activating and inhibiting the mTOR/p70S6K and the NF‐ κ B pathways. As apoptotic cells are crucial players of the innate immune signals initiating Th17 differentiation that induce TH17‐mediated immunity, thereby the findings by Di Giovangiulio et al . could be explained as ghrelin suppressing the intestinal cells apoptosis and in turn suppressing T‐cell‐mediated immunity.…”

Section: Ghrelin and Mechanistic Considerationsmentioning

confidence: 99%

“…T helper cells (Th) and their cytokine discovery provided a new distinguishing bridge for the communication between innate and adaptive immunity in GI inflammatory disorders. Considering that ghrelin and its receptor are expressed in T cells, Di Giovangiulio et al . demonstrated a unique protective effect of ghrelin in an experimental model of chronic intestinal inflammation through the modulation of the T‐cell immune response, suggesting a potential use for ghrelin in inflammatory bowel disease (IBD) patients.…”

Section: Introductionmentioning

confidence: 99%

“…Although most studies have shown that ghrelin plays an important role in appetite and metabolism, ghrelin has also been implicated in the inflammatory process, but its role is controversial. Here, we review the role of ghrelin in modulating intestinal immunity and inflammation and highlight its role in the pathology and pathophysiology of IBD and incorporate new data presented in this issue by Di Giovangiulio et al …”

Section: Introductionmentioning

confidence: 99%

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Immunomodulatory effect of ghrelin in the intestinal mucosa

Eissa

Ghia

2015

Neurogastroenterology Motil

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The gastrointestinal tract is the largest endocrine organ in the body and it produces a wide array of hormones and neuropeptides. Ghrelin, a 28-amino acid hormone produced mainly by the X/A-like endocrine cells in the gastric mucosa, has widespread tissue distribution and diverse physiological functions such as hormonal, orexigenic, metabolic, cardiovascular, neurological and immunological activities. Recent research has implicated ghrelin in gastrointestinal pathological conditions and immune system regulation, but its contribution is controversial. Although ghrelin levels are elevated in clinical active inflammatory bowel diseases, confirmation of its exact role using experimental models remains unclear. This review discusses the conflicting effects of ghrelin on intestinal inflammation, through the different possible immune and intracellular mechanisms and highlights new findings.

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Section: Ghrelin and Mechanistic Considerationssupporting

confidence: 53%

Section: Ghrelin and Mechanistic Considerationsmentioning

confidence: 99%

Section: Ghrelin and Mechanistic Considerationsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Immunomodulatory effect of ghrelin in the intestinal mucosa

Eissa

Ghia

2015

Neurogastroenterology Motil

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Neuroimmune Modulation of Gut Function

Shea‐Donohue

Urban

2016

Gastrointestinal Pharmacology

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Neuroimmune communications are facilitated by the production of neurotransmitters by immune cells and the generation of immune mediators by immune cells, which form a functional entity called the "neuroimmune synapse." There are several mechanisms that further facilitate neuroimmune interactions including the anatomic proximity between immune cells and nerves, the expression of receptors for neurotransmitters on immune cells and for immune mediators on nerves, and the receptor-mediated activation of intracellular signaling pathways that modulate nerve and immune phenotype and function. The bidirectional communication between nerves and immune cells is implicated in allostasis, a process that describes the continuous adaptation to an ever-changing environment. Neuroimmune interactions are amplified during inflammation by the influx of activated immune cells that significantly alter the microenvironment. In this context, the types of neurotransmitters released by activated neurons or immune cells can exert pro- or anti-inflammatory effects. Dysregulation of the enteric nervous system control of gastrointestinal functions, such as epithelial permeability and secretion as well as smooth muscle contractility, also contribute to the chronicity of inflammation. Persistent active inflammation in the gut leads to neuroimmune plasticity, which is a structural and functional remodeling in both the neural and immune systems. The importance of neuroimmune interactions has made them an emerging target in the development of novel therapies for GI pathologies.

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