Inflammatory Bowel Disease (IBD) & Sphingomyelin

Several studies have shown that inflammation can affect the sphingolipid salvage pathways. However, less is known about how inflammatory signals influence the regulation of de novo sphingolipid synthesis. Neutral sphingomyelinase 2 plays a role in controlling the inflammatory responses in monocytes and macrophages that are triggered by Tumor Necrosis Factor alfa (TNF-alfa). The inhibition of Acid sphingomyelinase reduces the release of inflammatory cytokines from macrophages triggered by lipopolysaccharides. It also offers protection against disease pathology in mice with colitis induced by dextran sulphate sodium.
Sakata et al. 2007 Immunology 122: 54-64
Al-Rashed et al. 2020 Sci Rep 10: 16802

Sphingolipid metabolism may be disrupted in Inflammatory Bowel Disease (IBD), resulting in an accumulation of specific Sphingolipids (e.g., Ceramides, sphingomyelin) that promote an inflammatory state.
Braun et al. 2009
Fischbeck et al. 2011
Qi et al. 2014

Dietary sphingomyelin was able to enhance apoptosis in intestinal epithelial cells in DSS colitis
Fischbeck et al. 2011

see also:
Inflammatory Bowel Disease (IBD) & Sphingolipids