Sphingosine-1-Phosphate Metabolism and Its Role in the Development of Inflammatory Bowel Disease
Holy Cross Oncology Center of Kielce, Artwińskiego 3, 25-734 Kielce, Poland
Department of Microbiology and Immunology, The Faculty of Health Sciences of the Jan Kochanowski University in Kielce, Aleja IX Wieków Kielc, 25-317 Kielce, Poland
Department of Microbiological and Nanobiomedical Engineering, Medical University of Białystok, 15-222 Białystok, Poland
Department of Hygiene, Epidemiology and Ergonomics, Medical University of Białystok, 15-230 Białystok, Poland
Author to whom correspondence should be addressed.
Academic Editor: Burkhard Kleuser
Int. J. Mol. Sci. 2017, 18(4), 741; https://doi.org/10.3390/ijms18040741
Received: 3 February 2017 / Revised: 20 March 2017 / Accepted: 27 March 2017 / Published: 31 March 2017
(This article belongs to the Special Issue Sphingolipids: Signals and Disease)
Beyond their role as structural molecules, sphingolipids are involved in many important cellular processes including cell proliferation, apoptosis, inflammation, and migration. Altered sphingolipid metabolism is observed in many pathological conditions including gastrointestinal diseases. Inflammatory bowel disease (IBD) represents a state of complex, unpredictable, and destructive inflammation of unknown origin within the gastrointestinal tract. The mechanisms explaining the pathophysiology of IBD involve signal transduction pathways regulating gastro-intestinal system’s immunity. Progressive intestinal tissue destruction observed in chronic inflammation may be associated with an increased risk of colon cancer. Sphingosine-1-phosphate (S1P), a sphingolipid metabolite, functions as a cofactor in inflammatory signaling and becomes a target in the treatment of IBD, which might prevent its conversion to cancer. This paper summarizes new findings indicating the impact of (S1P) on IBD development and IBD-associated carcinogenesis.