Abstract
Medium chain triglyceride (MCT) oil has been postulated to modulate inflammatory responses, but the detailed mechanisms have not been fully elucidated. Based on recent studies demonstrating that mitochondrial metabolic reprogramming and immune responses are correlated, the current study sought to determine whether MCT oil controls inflammatory responses through modulation of mitochondria using both in vitro and in vivo models. The mitochondrial metabolic phenotypes of macrophages were assessed according to oxygen consumption rate (OCR). Inflammatory responses were assessed for production of cytokines and expression of activation markers. MCT oil was more rapidly oxidized as observed by increased OCR in macrophages. The production of pro-inflammatory cytokines was down-regulated and anti-inflammatory cytokine was elevated by MCT oil. In addition, classically activated M1 and alternatively activated M2 markers were reciprocally regulated by MCT intervention. Overall, up-regulated β-oxidation by MCT contributes to the anti-inflammatory M2-like status of macrophages, which may aid in the dietary prevention and/or amelioration of inflammation.
Highlights
A number of recent studies have demonstrated that mitochondrial energy metabolism has a strong correlation with inflammatory responses, including macrophage polarization [1,2]
Cytotoxicity of canola or Medium chain triglyceride (MCT) oil emulsified in DMSO, as well as the vehicle itself, was determined by MTT assay
In non-stimulated conditions, oxygen consumption rate (OCR) of mitochondria were not more strongly affected by MCT oil compared to canola oil and non-oil-treated control (Figure 1A)
Summary
A number of recent studies have demonstrated that mitochondrial energy metabolism has a strong correlation with inflammatory responses, including macrophage polarization [1,2]. Classically activated M1 macrophages depend on glycolysis and further lactate fermentation, even in the presence of excess oxygen in cytoplasm. An extracellular flux analyzer was recently developed to quantify glycolysis and OXPHOS by real-time assessments of proton efflux and oxygen consumption, respectively, in the micromilieu of the cellular environment [4]. In accordance with the above-mentioned cellular energy metabolism, murine bone-marrow derived macrophages (non-polarized, M0) were successfully demonstrated to reciprocally regulate oxygen consumption in lipopolysaccharide (LPS) stimulated M1 vs interleukin (IL)-4/IL-13 induced M2 subsets [5].
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