- Research Article
- 10.1093/ecco-jcc/jjaf231.266
P0085 eNAMPT Shapes Myeloid Differentiation Programs of Hematopoietic Stem Cells in Crohn’s Disease
- Jan 01, 2026
- Journal of Crohn’s and Colitis
- C Travelli + 14 more +14
Abstract Background Nicotinamide phosphoribosyltransferase (NAMPT) is an essential and pleiotropic enzyme expressed in mammalian cells. Its intracellular form (iNAMPT) functions as the rate-limiting enzyme in the NAD+ salvage pathway. Through this activity, iNAMPT regulates cellular metabolism, mitochondrial biogenesis, and adaptive responses to inflammation and oxidative stress. In contrast, extracellular NAMPT (eNAMPT), secreted by multiple cell types including immune cells, acts as a pro-inflammatory cytokine and contributes to several inflammation-driven disorders such as inflammatory bowel disease (IBD). The mechanisms governing eNAMPT secretion and receptor engagement remain incompletely understood; to date, TLR4 is the only receptor that has been identified. Notably, circulating eNAMPT levels are elevated during active disease phases and negatively correlate with responsiveness to anti-TNF therapy (Colombo et al., 2020, 2022).We investigated the mechanistic contribution of eNAMPT to Crohn’s disease (CD) progression using the DNBS-induced colitis model. Methods BALB/c mice received intrarectal DNBS (2 mg for moderate or 3 mg for severe inflammation) and were treated daily with recombinant eNAMPT (50 µg/mouse) to mimic the elevated systemic levels observed in CD patients. Colon, blood, bone marrow were collected for flow cytometry, bulkRNAseq, array, RT-PCR and IHC. Results eNAMPT administration exacerbated disease severity, as evidenced by increased weight loss, colon shortening, and aggravated epithelial and mucosal damage on H&E, Picrosirius Red, and Masson’s Trichrome staining. eNAMPT further enhanced fibroblast activation, collagen deposition, and inflammatory scores. Flow cytometric analyses of the lamina propria revealed increased CD11b+ myeloid infiltration and an immature Ly6G+ granulocytes. phenotype. eNAMPT treatment in moderate colitis promoted a significant expansion of the Lin-c-Kit+ hematopoietic compartment (similar to the DSS model), reaching levels comparable to severe DNBS inflammation. This was accompanied by a selective increase in GMPs indicating skewing toward myelopoiesis. In vitro, NAMPT alone showed minimal pro-myelopoietic activity; however, its combination with IL-6 or G-CSF modestly enhanced colony formation, and a synergistic effect was observed with GM-CSF. Finally, the pathogenic activity of eNAMPT was abolished in TLR4-deficient mice, indicating a TLR4-dependent mechanism. Conclusion Collectively, these findings demonstrate that the cytokine eNAMPT exacerbates Crohn’s disease by acting along the gut–bone marrow axis, promoting HSC proliferation and differentiation toward immature granulocytes that infiltrate the colon and intensify fibrotic remodeling.
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