ArticleFrontiers in immunology2026
Chemokine-receptor-dependent inflammatory responses contribute to two-hit-induced experimental necrotizing enterocolitis and represent a potential therapeutic target.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Necrotizing enterocolitis (NEC) is a severe multifactorial inflammatory disorder of the preterm intestine for which effective preventive and therapeutic strategies remain limited. Using formula feeding (FF)-associated dysbiosis combined with subsequent viral inflammation, we previously demonstrated that this clinically relevant two-hit strategy induces NEC through a complex mechanism involving the Methods: NEC was induced in C57BL/6 mouse pups using two novel and clinically relevant two-hit models: FF combined with R837-triggered viral inflammation, or TV gavage in dam-fed pups followed by R837 treatment. In some experiments, pups were pretreated subcutaneously with TAK-779, a pharmacologic inhibitor of CCR2/CCR5/CXCR3 signaling. NEC-like intestinal injury was assessed by intestinal permeability and histological analysis. RT-qPCR and flow cytometry were used to evaluate chemokine-receptor expression and inflammatory cell infiltration, respectively. A human NEC RNA-seq dataset (E-MTAB-15683) was used to evaluate the expression of chemokine-receptor genes. Results: Following the R837-induced second hit, mouse pups previously subjected to the FF-associated first hit exhibited robust induction of chemokines and chemokine receptors, accompanied by recruitment of inflammatory cells and the development of NEC. TAK-779 markedly reduced the expression of chemokines and their receptors, attenuated inflammatory cell recruitment, and protected against NEC induced by the sequential FF- and viral inflammation-associated two-hit process. Similarly, subjecting BF pups to TV (first hit) followed by R837 treatment (second hit) resulted in heightened expression of chemokines and their receptors, accompanied by NEC development; both effects were prevented by TAK-779 pretreatment. Notably, analysis of human NEC transcriptomic data revealed increased expression of multiple chemokines and chemokine receptors in diseased intestinal tissues. Conclusions: Our findings demonstrate that chemokine-receptor-dependent inflammatory responses contribute to the propagation of NEC by promoting the accumulation of NK1.1
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