ArticleEuropean journal of medical research2025
Targeting CXCL8 alleviates intestinal epithelial inflammation by suppressing the JAK-STAT pathway.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Ruxolitinib reverses alopecia areata via a triple mechanism: JAK-STAT inhibition, localized oxidative stress attenuation and selective apoptosis modulation.Journal of translational autoimmunity · 2026Article
- Intestinal epithelial cell-specific deletion of Jak2 disrupts gut homeostasis.Scientific reports · 2026Article
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Authors and funding
7 authors.
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Abstract
backgroundInhibition of CXCL8 has been shown to alleviate small intestinal inflammation and suppress activation of Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway. However, the mechanism of the interaction between the two requires further exploration.
methodsHuman small intestinal epithelial cells were stimulated with lipopolysaccharide (LPS) to establish an inflammatory model. The expression of pro-inflammatory factors was detected using qRT-PCR. Cell viability and apoptosis in cells treated with LPS or phosphate buffered saline (PBS) were assessed by CCK-8 assay and flow cytometry, respectively. Western blot was conducted to detect the expression of proteins linked to the JAK-STAT signaling pathway. Then, cell viability, apoptosis, and the expression of JAK-STAT pathway-associated protein were compared between si-CXCL8#1 and si-NC groups. Furthermore, after overexpressing STAT1 in si-CXCL8#1 group, changes in pro-inflammatory cytokine level, cell viability, and apoptosis were analyzed.
resultsCompared to the PBS control, LPS stimulation significantly increased apoptosis, promoted the release of pro-inflammatory mediators, upregulated JAK-STAT pathway protein expression, and reduced cell viability. CXCL8 silencing (si-CXCL8#1) enhanced cell viability, suppressed the release of pro-inflammatory mediators, decreased apoptosis, and downregulated the level of JAK-STAT signaling protein levels. Importantly, in comparison to the si-CXCL8#1 + oe-NC group, the apoptosis and expression of pro-inflammatory mediators were significantly elevated and cell viability was reduced in the si-CXCL8#1 + oe-STAT1 group.
conclusionThis study revealed that CXCL8 aggravated inflammation in small intestinal epithelial cells by activating the JAK-STAT pathway. Silencing CXCL8 alleviated LPS-induced inflammation and improved cell survival, which were reversed by STAT1 overexpression. These results highlighted the CXCL8-JAK-STAT axis as a potential therapeutic target for treating IBDs such as Crohn's disease.
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