Macrophage SELENOP controls neutrophil homeostasis through redox stress regulation in Crohn's disease.

What To Know

This study (abstract) reports that macrophage-derived SELENOP is reduced in inflamed colon tissue from people with Crohn’s disease and that loss of macrophage SELENOP promotes oxidative stress, neutrophil activation (including NET formation), and worse inflammation in experimental colitis models.

Mechanistic work in cells and mice implicated ubiquitin-mediated degradation of SELENOP and downstream antioxidant signaling (SESN2/NRF2) as contributors to macrophage pro-oxidative states.

The authors performed single-cell RNA sequencing on human colon samples, in vitro macrophage–neutrophil assays, and mouse models where SELENOP was deleted in myeloid cells or overexpressed. Myeloid SELENOP loss worsened TNBS colitis, while SELENOP overexpression ameliorated inflammation in IL-10–deficient mice, supporting a causal role in preclinical models.

This is a mechanistic/basic-science report that suggests macrophage SELENOP is a potential redox checkpoint and a possible therapeutic target to limit oxidative-stress–driven inflammation in Crohn’s disease. It does not provide clinical trial data or ready-to-use therapies.