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Multiomic analysis reveals a role of Fusobacterium periodonticum in colorectal tumorigenesis by decanoic acid promoting neutrophil chemotaxis

ABSTRACT: Gut microbiota dysbiosis and immune dysregulation are closely linked to colorectal cancer development. Identifying mechanistic connections among specific microbial species, metabolites, and immune responses may reveal novel insights into its pathogenesis. Here, employing metagenomic, metabolomic, and single-cell transcriptomic analyses across clinical cohorts, we identify Fusobacterium periodonticum as significantly enriched in colorectal cancer patients and strongly correlated with elevated decanoic acid levels, and further reveal tissue-specific neutrophil enrichment in colorectal cancer. Cellular experiments demonstrate that decanoic acid induces neutrophil late apoptosis/necrosis and enhances chemotaxis through a pertussis toxin-sensitive G-protein-dependent mechanism, while upregulating genes associated with leukocyte migration and tumorigenesis. Mouse models further confirm that F. periodonticum colonization increases dysplasia and decanoic acid levels, and that decanoic acid intervention promotes tumor progression through neutrophil infiltration and immune modulation. Our study reveals an important role of F. periodonticum in colorectal tumorigenesis via decanoic acid-medicated neutrophil chemotaxis, providing new insights into colorectal cancer pathogenesis

INSTRUMENT(S): Liquid Chromatography MS - positive - hilic, Liquid Chromatography MS - negative - hilic

PROVIDER: MTBLS14505 | MetaboLights | 2026-05-20

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS14505_LC-MS_negative_hilic.txt	Txt
	a_MTBLS14505_LC-MS_positive_hilic.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS14505_LC-MS_negative_hilic_v2_maf.tsv	Tabular
	m_MTBLS14505_LC-MS_positive_hilic_v2_maf.tsv	Tabular

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Project description:Necrotic enteritis is a disease caused by Clostridium perfringens, which threatens poultry production in the absence of dietary antibiotics. A total number of 144 Ross broilers were reared in 12 pens with each hosting 12 birds. Each 6 pens of birds were fed medicated (bacitracin at 55 ppm) or non-medicated starter diets (Nutreco Canada Agresearch) immediately after the chicks were placed. At day 18, birds were challenged with C. perfringens (107 cfu per ml mixed with feed). Spleens were collected from 12 birds of each group at day 18 (before infection), 19, 20, and 22. A low-density chicken immune microarray was used to study gene expression profiling of host response to C. perfringens infection. Six biological replicates (2 birds per biological replicate) for each treatment group were labeled with either Cy5 or Cy3 with dye swap. A total of 24 arrays were used for this study. Gene signal intensity was globally normalized by LOWESS and expressed as log2 ratios. A mixed model including treatment, time, array, subgrid (random effect), dye, and all interactions among treatment and time was used to identify differentially expressed genes between post-infection vs. pre-infection, among post-infections, and between medication treatments, at the 5% significance level. The results indicated subtle medication effects on gene expression of these immune-related genes compared to bacterial infection effect. Our findings strongly suggest that both cell-mediated and antibody-mediated immune responses via MHC class I and II systems were actively involved in the host defense against C. perfringens infection in broilers. The unique cytokine signaling pathway and apoptosis cascade found in the study provide a new insight of molecular regulation of host immune response. Collectively, the findings of the present study will shed light on the molecular mechanisms underlying C. perfringens infection in broilers. There were two groups: medicated and non-medicated. Spleen were collected to isolate total RNA for gene expression profiling.For the microarray study, two birds from each pen were pooled within each group. To account for any bias inherent to the fluorescent dyes, three of the six medicated replicates were labeled with Cy3 and the other three were labeled with Cy5 at each time point. The same design was applied for the non-medicated group. There were six hybridizations between medicated and non-medicated replicates at each time point. Twenty-three out of 24 arrays were used (data from one array were discarded due to poor quality).

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Multiomic analysis reveals a role of Fusobacterium periodonticum in colorectal tumorigenesis by decanoic acid promoting neutrophil chemotaxis

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