The Role of Neuropeptides in Mouse Models of Colitis

Padua, David; Vu, John P.; Germano, Patrizia M.; Pisegna, Joseph R.

doi:10.1007/s12031-015-0688-1

Cited by 22 publications

(21 citation statements)

References 72 publications

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“…The immunohistochemical examination and quantification of tissue extracts from rectal biopsy samples obtained from patients with UC and CD showed an increased number of VIP-positive nerve fibers and an increased VIP concentration in CD but not in UC[ 253 ]. Other studies found that the number of VIP - positive nerve fibers was either decreased or unchanged in patients with UC and CD[ 245 , 254 , 255 ]. These contradictory results for VIP in patients with IBD could be explained by VIP occurring mostly in neurons of the ENS and that analyzing VIP in small mucosal biopsy specimens obtained during an endoscopic examination does not produce reliable results.…”

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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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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“…DSS is a water soluble, negatively charged sulfated polysaccharide with a highly variable molecular weight. The exact mechanism of DSS‐induced colitis is not clearly defined, but its major effect is disruption of the intestinal barrier integrity leading to intestinal inflammation . The severity of the resulting colitis can be altered by many factors including, but not limited to the strain or gender of the animal or the molecular weight of DSS selected .…”

Section: Introductionmentioning

confidence: 99%

Weight loss is a sufficient and economical single outcome measure of murine dextran sulfate sodium colitis

2019

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Inflammatory bowel diseases (IBD: Crohn's disease and ulcerative colitis) are becoming common around the world without a cure. Animal models of colitis have become instrumental in IBD research. The dextran sulfate sodium (DSS) induced murine colitis model is likely the most utilized due to its simplicity and reproducibility with over 4000 publications on PubMed, where weight loss is the most commonly used and reliable positive correlate. We predicted at current state of art, that the DSS colitis model can be optimized by using weight loss as a single cost‐saving outcome measure. Twenty recent and consecutive publications using the DSS model in PubMed were selected for review. Guarded cost estimations for additional outcome measures of colitis beyond weight loss were performed. In all manuscripts (100%), weight loss corroborated the conclusions. Average excess cost for examining additional measures of colitis was approximately $6700 per publication. Two studies (10.5%) were estimated to have spent over $20,000 in excess. Additional measures of colitis either supported the final conclusions found with weight loss, or lead to indeterminate results. Potential annual savings from following our guidance were calculated to be over $60,000 for and IBD lab. We conclude that weight loss is a sufficient, objective, and economical outcome measure of DSS‐induced colitis in mice.

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“…Pituitary adenylate cyclase activating polypeptide (PACAP) is the most conserved member of the vasoactive intestinal peptide (VIP)/PACAP/glucagon superfamily [1][2][3][4]. Since its discovery in 1989 by Miyata and co-workers [5] in hypothalamus, numerous functions have been attributed to PACAP in addition to its adenylate cyclase activation in pituitary cells.…”

Section: Text: Introductionmentioning

confidence: 99%

Protective Role of Endogenous PACAP in Inflammation-induced Retinal Degeneration

Vaczy

Kovari

Kovács

et al. 2018

CPD

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Purpose. Pituitary adenylate cyclase activating polypeptide (PACAP) is a neuroprotective peptide that has been shown to exert protective effects in different models of neurodegenerative diseases, including retinal degenerations. Data obtained from PACAPdeficient (PACAP KO) mice provide evidence that endogenous PACAP has neuroprotective role in different pathologies. PACAP KO mice show enhanced sensitivity to different insults, such as oxidative stress, hypoxia and inflammation. The aim of the present study was to investigate the protective effects of endogenous PACAP in retinal inflammation. Methods. Endotoxin-caused eye inflammation was induced by intraperitoneal injection of lipopolysaccharide (LPS) in PACAP KO and wild type (Wt) mice. After LPS treatment, retinas were processed for histological examination. To detect the alterations of different proteins and cytokines, immunohistochemical, western blot and cytokine array were used. We also performed dark-adapted electroretinography (ERG) to detect the functional differences. Results. The thickness of nearly all layers was significantly less in LPS-injected PACAP KO mice compared to Wt animals. Increased expression of glial fibrillary acidic protein (GFAP) was induced in Müller glial cells after LPS treatment, which was more intense in PACAP KO mice. The levels of pAkt and pGSK were decreased in PACAP KO group during inflammation. LPS treatment significantly increased cytokines (sICAM-1, JE, TIMP-1) in both treated groups, but it was more expressed in PACAP KO animals. Furthermore, ERG responses were disturbed after LPS injection in PACAP KO mice. Conclusion. Our results showed that endogenous PACAP has a protective role in LPS-caused retinal inflammation.

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The Role of Neuropeptides in Mouse Models of Colitis

Cited by 22 publications

References 72 publications

Gastrointestinal neuroendocrine peptides/amines in inflammatory bowel disease

Gastrointestinal neuroendocrine peptides/amines in inflammatory bowel disease

Weight loss is a sufficient and economical single outcome measure of murine dextran sulfate sodium colitis

Protective Role of Endogenous PACAP in Inflammation-induced Retinal Degeneration

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