High-fat diet promotes colorectal tumorigenesis through gut microbiota-mediated metabolic reprogramming and M2 macrophage polarization.
1/5 보강
PICO 자동 추출 (휴리스틱, conf 2/4)
유사 논문P · Population 대상 환자/모집단
추출되지 않음
I · Intervention 중재 / 시술
12-weeks HFD
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
massiliensis) or glycan hydrolysis pathways (e.g. GH95 enzyme) may provide mechanism-guided anti-CRC strategies.
[BACKGROUND] High-fat diet (HFD) drives colorectal cancer (CRC) progression through gut microbiota dysbiosis and M2 macrophage polarization, yet the microbiota-immunity crosstalk remains mechanistical
- 표본수 (n) 8
APA
Xu L, Zhang J, et al. (2026). High-fat diet promotes colorectal tumorigenesis through gut microbiota-mediated metabolic reprogramming and M2 macrophage polarization.. Biochemical and biophysical research communications, 794, 153014. https://doi.org/10.1016/j.bbrc.2025.153014
MLA
Xu L, et al.. "High-fat diet promotes colorectal tumorigenesis through gut microbiota-mediated metabolic reprogramming and M2 macrophage polarization.." Biochemical and biophysical research communications, vol. 794, 2026, pp. 153014.
PMID
41297516
Abstract
[BACKGROUND] High-fat diet (HFD) drives colorectal cancer (CRC) progression through gut microbiota dysbiosis and M2 macrophage polarization, yet the microbiota-immunity crosstalk remains mechanistically unresolved.
[METHODS] APC (CRC model, n = 8) and wild-type controls (n = 7) received 12-weeks HFD. We employed integrated metagenomic sequencing (Illumina NovaSeq) and immunohistochemistry (targeting CD206+ M2 macrophages) to investigate the linkages between the gut microbiota and the host.
[RESULTS] CRC mice exhibited colonic adenocarcinoma with increased M2 macrophages. Gut microbiota in CRC mice showed enrichment of pro-inflammatory taxa (e.g., Bacteroides massiliensis, Vampirovibrion) and upregulated pathways (carbohydrate metabolism, mucin degradation). Strikingly, the relative abundances of Bacteroides massiliensis and Vampirovibrion showed significant positive correlations with CD206+ M2 macrophage infiltration levels.
[CONCLUSION] HFD induces microbiota-directed metabolic reprogramming and M2 polarization, synergistically accelerating CRC. Notably, targeting key pro-inflammatory taxa (e.g., B. massiliensis) or glycan hydrolysis pathways (e.g. GH95 enzyme) may provide mechanism-guided anti-CRC strategies.
[METHODS] APC (CRC model, n = 8) and wild-type controls (n = 7) received 12-weeks HFD. We employed integrated metagenomic sequencing (Illumina NovaSeq) and immunohistochemistry (targeting CD206+ M2 macrophages) to investigate the linkages between the gut microbiota and the host.
[RESULTS] CRC mice exhibited colonic adenocarcinoma with increased M2 macrophages. Gut microbiota in CRC mice showed enrichment of pro-inflammatory taxa (e.g., Bacteroides massiliensis, Vampirovibrion) and upregulated pathways (carbohydrate metabolism, mucin degradation). Strikingly, the relative abundances of Bacteroides massiliensis and Vampirovibrion showed significant positive correlations with CD206+ M2 macrophage infiltration levels.
[CONCLUSION] HFD induces microbiota-directed metabolic reprogramming and M2 polarization, synergistically accelerating CRC. Notably, targeting key pro-inflammatory taxa (e.g., B. massiliensis) or glycan hydrolysis pathways (e.g. GH95 enzyme) may provide mechanism-guided anti-CRC strategies.
MeSH Terms
Gastrointestinal Microbiome; Animals; Diet, High-Fat; Macrophages; Colorectal Neoplasms; Mice; Mice, Inbred C57BL; Carcinogenesis; Male; Metabolic Reprogramming
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