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Cited by 42Polyamine Metabolism and ApplicationsSepsis Diagnosis and TreatmentNitric Oxide and Endothelin Effects

The DOI matches its Crossref record.

ORAL SPERMINE ADMINISTRATION INHIBITS NITRIC OXIDE-MEDIATED INTESTINAL DAMAGE AND LEVELS OF SYSTEMIC INFLAMMATORY MEDIATORS IN A MOUSE ENDOTOXIN MODEL

ter Steege, J. C.A., Forget, P. Ph., Buurman, W. A.·1999·Shock
DOI 10.1097/00024382-199902000-00008
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Abstract

Enhanced intestinal nitric oxide production observed during sepsis is thought to play a central role in lipopolysaccharide-induced intestinal damage. In contrast intestinal polyamines, both from endogenous and exogenous origin, are essential for the maintenance of mucosal integrity. Polyamines have been shown to inhibit lipopolysaccharide-induced nitric oxide release in vitro and have been claimed to exert additional antiinflammatory actions. In this study, the effect of the polyamine spermine on the release of the proinflammatory mediators nitric oxide and tumor necrosis factor-alpha by a murine macrophage cell line was investigated. Furthermore, we investigated whether oral spermine administration inhibits lipopolysaccharide-induced intestinal inducible nitric oxide synthase and nitrotyrosine expression and modulates the release of inflammatory mediators. Our results show that although spermine inhibited lipopolysaccharide-induced nitric oxide release in a murine macrophage cell line, no effect on tumor necrosis factor-alpha release was observed. In addition, oral spermine administration inhibited intestinal inducible nitric oxide synthase and nitrotyrosine expression suggesting a protective effect of spermine on lipopolysaccharide-induced intestinal damage. In parallel a decrease in serum levels of the proinflammatory mediators nitrate, nitrite, and interferon-gamma and an increase in the antiinflammatory cytokine interleukin-10 was observed, although tumor necrosis factor-alpha levels were unaffected. These results indicate that spermine inhibits lipopolysaccharide-induced nitric oxide release in vitro as well as in vivo. Further, intraluminally derived polyamines modulate the systemic immune response. It is concluded that oral spermine administration might have therapeutic perspectives for several disorders characterized by systemic inflammation and intestinal damage.

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Metadata

Authors
ter Steege, J. C. A., Forget, P. P., & Buurman, W. A.
Affiliations
  • Maastricht University Medical Centre (NL)
  • Maastricht University (NL)
Corresponding author
Forget, P. Ph.
ORCID
Buurman, W. A.
Venue
Shock
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1999-02
Volume
11
Issue
2
Pages
115-119
ISSN
1073-2322 (ISSN-L)
DOI
10.1097/00024382-199902000-00008
OpenAlex
W2029884739
Cited by
42
References
0
Citations by year
2026: 1 · 2022: 1 · 2021: 2 · 2020: 1 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 2 · 2013: 3 · 2012: 3
FWCI
0.80
Type
journal article
Language
en
Open access
closed
Locations
  • Shock (publishedVersion)
  • PubMed (publishedVersion)
  • Research Publications (Maastricht University) (publishedVersion)
  • Research Publications (Maastricht University) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Polyamine Metabolism and Applications
  • Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Sepsis Diagnosis and Treatment
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Keywords
spermine, polyamines, nitric oxide, lipopolysaccharide, endotoxemia, intestinal injury, inducible nitric oxide synthase, nitrotyrosine, TNF-α, macrophages, interferon-gamma, IL-10, systemic inflammation, sepsis, oral administration, intestinal mucosal integrity
MeSH terms
Administration, Oral, Animals, Disease Models, Animal, Escherichia coli, Female, Immunohistochemistry, Inflammation, Interferon-gamma, Intestinal Mucosa, Intestines, Lipopolysaccharides, Macrophages, Neutrophils, Nitrates, Nitric Oxide, Nitrites, Shock, Septic, Spermine, Tumor Necrosis Factor-alpha, Tyrosine, Interleukin-10, Nitric Oxide Synthase, Mice, Nitric Oxide Synthase Type II

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