Macrophage‐derived CD38 mediates colitis through NAD + depletion

What To Know

This Journal of Physiology study (abstract available) reports that colitis in experimental models is associated with disrupted NAD+ metabolism and increased expression of CD38, primarily in infiltrating macrophages.

Restoring NAD+ levels—either by supplementing precursors such as nicotinamide mononucleotide or by pharmacologically inhibiting CD38—or deleting Cd38 in myeloid cells reduced metabolic disturbances and improved colitis measures in the reported experiments.

The authors highlight a mechanistic link between macrophage CD38 activity, NAD+ depletion, and intestinal inflammation, and suggest the CD38/NAD+ axis as a potential therapeutic target for IBD.

The report is based on preclinical experimental work (including genetic deletion and drug interventions) summarized in the article abstract, not on human clinical trials. If you are reading because of personal IBD: this is early-stage laboratory research that identifies a possible new pathway for treatment development.

It does not establish safety or effectiveness of any specific NAD+-boosting supplements or CD38 inhibitors in people with IBD.

For clinicians and researchers: the paper supports further preclinical and translational work on macrophage CD38 and NAD+ metabolism in intestinal inflammation; confirmatory studies and clinical testing would be needed before changes to care.