N-glycosylation negatively regulates the expression of tumor necrosis factor (TNF) in mouse macrophage.

Tumor necrosis factor alpha (TNF) is a potent inflammatory cytokine and is also involved in the pathogenesis of various diseases such as inflammatory bowel disease and rheumatoid arthritis. While the intracellular signal cascades of TNF stimulation have been extensively studied, the regulatory mechanism of TNF production is still largely unknown. In this study, we investigated the role of N-glycosylation of TNF in its production.

A potent endocytosis inhibitor Ikarugamycin up-regulates TNF production.

Ikarugamycin (IK) is an antibiotic which has been reported to have a variety of functions, such as inhibition of clathrin-mediated endocytosis (CME), anti-tumor effects and regulation of the immune system. Whether IK influences cytokine production is poorly understood. We have investigated the relationship between IK and production of tumor necrosis factor-α (TNF).

Oral administration of D-serine prevents the onset and progression of colitis in mice.

Background: L-amino acids are the predominant forms of organic molecules on the planet, but recent studies have revealed that various foods contain D-amino acids, the enantiomers of L-amino acids. Though diet plays important roles in both the development and progression of inflammatory bowel disease (IBD), to our best knowledge, there has been no report on any potential interactions between D-amino acids and IBD. In this report, we aim to assess the effects of D-serine in a murine model of IBD.