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CLA-supplemented diet accelerates experimental colorectal cancer by inducing TGF-β-producing macrophages and T cells
- Source :
- Mucosal Immunology. 12:188-199
- Publication Year :
- 2019
- Publisher :
- Elsevier BV, 2019.
-
Abstract
- Conjugated linoleic acid (CLA) has been shown to activate the nuclear receptor PPAR-γ and modulate metabolic and immune functions. Despite the worldwide use of CLA dietary supplementation, strong scientific evidence for its proposed beneficial actions are missing. We found that CLA-supplemented diet reduced mucosal damage and inflammatory infiltrate in the dextran sodium sulfate (DSS)-induced colitis model. Conditional deletion of PPAR-γ in macrophages from mice supplemented with CLA diet resulted in loss of this protective effect of CLA, suggesting a PPAR-γ-dependent mechanism mediated by macrophages. However, CLA supplementation significantly worsened colorectal tumor formation induced by azoxymethane and DSS by inducing macrophage and T-cell-producing TGF-β via PPAR-γ activation. Accordingly, either macrophage-specific deletion of PPAR-γ or in vivo neutralization of latency-associated peptide (LAP, a membrane-bound TGF-β)-expressing cells abrogated the protumorigenic effect of CLA. Thus, the anti-inflammatory properties of CLA are associated with prevention of colitis but also with development of colorectal cancer.
- Subjects :
- 0301 basic medicine
chemistry.chemical_classification
integumentary system
Chemistry
Azoxymethane
Conjugated linoleic acid
Immunology
food and beverages
Peroxisome proliferator-activated receptor
medicine.disease
medicine.disease_cause
03 medical and health sciences
chemistry.chemical_compound
030104 developmental biology
0302 clinical medicine
Immune system
medicine
Cancer research
Immunology and Allergy
Macrophage
lipids (amino acids, peptides, and proteins)
Colitis
Carcinogenesis
030215 immunology
Transforming growth factor
Subjects
Details
- ISSN :
- 19330219
- Volume :
- 12
- Database :
- OpenAIRE
- Journal :
- Mucosal Immunology
- Accession number :
- edsair.doi...........f59e3fcc4a0b8109c8802ccdd5791fb2