Targeted deletion of neuropeptide Y (NPY) modulates experimental colitis
Open accessAbstract
BACKGROUND: Neurogenic inflammation plays a major role in the pathogenesis of inflammatory bowel disease (IBD). We examined the role of neuropeptide Y (NPY) and neuronal nitric oxide synthase (nNOS) in modulating colitis. METHODS: Colitis was induced by administration of dextran sodium sulphate (3% DSS) or streptomycin pre-treated Salmonella typhimurium (S.T.) in wild type (WT) and NPY (NPY(-/-)) knockout mice. Colitis was assessed by clinical score, histological score and myeloperoxidase activity. NPY and nNOS expression was assessed by immunostaining. Oxidative stress was assessed by measuring catalase activity, glutathione and nitrite levels. Colonic motility was assessed by isometric muscle recording in WT and DSS-treated mice. RESULTS: DSS/S.T. induced an increase in enteric neuronal NPY and nNOS expression in WT mice. WT mice were more susceptible to inflammation compared to NPY(-/-) as indicated by higher clinical & histological scores, and myeloperoxidase (MPO) activity (p<0.01). DSS-WT mice had increased nitrite, decreased glutathione (GSH) levels and increased catalase activity indicating more oxidative stress. The lower histological scores, MPO and chemokine KC in S.T.-treated nNOS(-/-) and NPY(-/-)/nNOS(-/-) mice supported the finding that loss of NPY-induced nNOS attenuated inflammation. The inflammation resulted in chronic impairment of colonic motility in DSS-WT mice. NPY -treated rat enteric neurons in vitro exhibited increased nitrite and TNF-alpha production. CONCLUSIONS: NPY mediated increase in nNOS is a determinant of oxidative stress and subsequent inflammation. Our study highlights the role of neuronal NPY and nNOS as mediators of inflammatory processes in IBD.
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In a colitis disease model, it was found that an increase in the colonic synthesis of NPY was associated with decreased colonic Y1 receptor expression.
“For example, in a colitis disease model, it was found that an increase in the colonic synthesis of NPY was associated with decreased colonic Y 1 receptor expression [208,209].”
From Anxiety, depression, and the microbiome: A role for gut peptides (2018) · cites this paper as [208]
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- Authors
- Chandrasekharan, B., Bala, V., Kolachala, V. L., Vijay-Kumar, M., Jones, D., Gewirtz, A. T., Sitaraman, S. V., & Srinivasan, S.
- Affiliations
- Emory University (US)
- Corresponding author
- Srinivasan, Shanthi
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2008-10-01
- Volume
- 3
- Issue
- 10
- Pages
- e3304
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC2561053
- OpenAlex
- W2074537715
- Cited by
- 70
- References
- 37
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 6 · 2021: 5 · 2020: 4 · 2019: 7 · 2018: 4 · 2017: 4 · 2016: 5 · 2015: 4 · 2014: 5 · 2013: 5 · 2012: 3
- FWCI
- 2.09
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Crohn's and Colitis Foundation of America
- National Institutes of Health (DK06411)
- National Institute of Diabetes and Digestive and Kidney Diseases (R03DK078552, R24DK064399, DK 06411, DK 064399, KO8 DK067045, K08DK067045)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- neuropeptide Y, neuronal nitric oxide synthase, experimental colitis, inflammatory bowel disease, neurogenic inflammation, oxidative stress, enteric neurons, colonic motility, Salmonella typhimurium, nitric oxide, TNF-α
- MeSH terms
- Animals, Catalase, Colitis, Disease Models, Animal, Glutathione, Inflammation, Peroxidase, Neuropeptide Y, Nitrites, Inflammatory Bowel Diseases, Dextran Sulfate, Gene Deletion, Mice, Knockout, Oxidative Stress, Mice, Nitric Oxide Synthase Type I
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