Peer-reviewed veterinary case report
How S1P signaling affects intestinal IgA in dogs with inflammatory
By Nakazawa, Maho et al.·Published in The Journal of veterinary medical science·2019·Department of Veterinary Clinical Pathobiology, Japan·View original on PubMed →
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Original publication title: Sphingosine-1-phosphate (S1P) signaling regulates the production of intestinal IgA and its potential role in the pathogenesis of canine inflammatory bowel disease.
- Species:
- dog
Plain-English summary
A study found that dogs with inflammatory bowel disease (IBD) may have lower levels of a specific molecule called sphingosine-1-phosphate (S1P), which is important for producing a type of antibody called immunoglobulin A (IgA) in the intestines. In healthy dogs, S1P helps regulate IgA production, but when researchers blocked S1P signaling in healthy dogs, they noticed a significant drop in IgA levels. This suggests that dogs with IBD might struggle to produce enough IgA due to decreased S1P levels, which could contribute to their gastrointestinal issues. Understanding this connection could help in developing better treatments for dogs suffering from IBD.
People also search for: dog inflammatory bowel disease treatment · low IgA in dogs · canine IBD symptoms · sphingosine-1-phosphate for dogs
Abstract
Inflammatory bowel disease (IBD) is a common gastrointestinal disease in dogs. Decreased production of intestinal immunoglobulin A (IgA) has been suggested as a possible pathogenesis in a subset of canine IBD; however, the underlying cause remains unclear. Sphingosine-1-phosphate (S1P) is a lipid mediator that regulates intestinal IgA production by controlling lymphocyte trafficking in mice. The objectives of this study were to clarify the role of S1P in IgA production in dogs and to evaluate the expression of S1P-related molecules in dogs with IBD. First, an S1P receptor antagonist was administrated to five healthy dogs. The S1P receptor antagonist significantly decreased the IgA concentration in sera and feces but did not affect the IgG concentration. Moreover, the immunoreactivity of intestinal IgA was significantly decreased by S1P signal blockade. These results indicate that S1P signaling specifically regulates the intestinal IgA production in dogs. Subsequently, the intestinal S1P concentration and the expression of S1P-related molecules were measured in dogs with IBD and healthy dogs. The intestinal concentration of S1P was significantly lower in dogs with IBD than in healthy dogs. In addition, the gene expression levels of S1P receptor (S1P1) and S1P synthase (SK1) were significantly lower in dogs with IBD than in healthy dogs. Taken together, these observations suggest that decreased S1P production, likely caused by a lower expression of S1P synthetase, leads to attenuation of S1P/S1P1 signaling pathway and the production of intestinal IgA in dogs with IBD.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/31341112/