Dietary coconut oil ameliorates skin contact hypersensitivity through mead acid production in mice

Abstract

Coconut oil is used as a dietary oil worldwide, and its healthy effects are recognized by the fact that coconut oil is easy to digest, helps in weight management, increases healthy cholesterol, and provides instant energy. Although topical application of coconut oil is known to reduce skin infection and inflammation, whether dietary coconut oil has any role in decreasing skin inflammation is unknown. In this study, we showed the impact of dietary coconut oil in allergic skin inflammation by using a mouse model of contact hypersensitivity (CHS). Mice maintained on coconut oil showed amelioration of skin inflammation and increased levels of cis-5, 8, 11-eicosatrienoic acid (mead acid) in serum. Intraperitoneal injection of mead acid inhibited CHS and reduced the number of neutrophils infiltrating to the skin. Detailed mechanistic studies unveiled that mead acid inhibited the directional migration of neutrophils by inhibiting the filamentous actin polymerization and leukotriene B 4 production required for secondary recruitment of neutrophils. Our findings provide valuable insights into the preventive roles of coconut oil and mead acid against skin inflammation, thereby offering attractive therapeutic possibilities. K E Y W O R D S coconut oil, LTB 4 , mead acid, neutrophils, skin inflammation | 1523 TIWARI eT Al.

Diet‐induced obesity aggravates NK cell–mediated contact hypersensitivity reaction in Rag1−/− mice

“…These discrepancies may arise from various factor, for example, the type of dietary oil used in the experiment. As shown before, different dietary fats have distinct effects on the immune response, including CHS reaction 34 . Here, we show that DIO exacerbates CHS response to DNFB in Rag1 −/− mice.…”

Dietary Omega-3 Fatty Acid Dampens Allergic Rhinitis via Eosinophilic Production of the Anti-Allergic Lipid Mediator 15-Hydroxyeicosapentaenoic Acid in Mice

“…The 18-HEPE is further transformed to resolvin E1 by 5-LOX expressed on neutrophils [42,43]. We also recently showed that neutrophil 5-LOX contributes to the production of leukotriene B 4 from ARA and influences the development of inflammation [26].…”

“…Neutrophils were collected from bone marrow cells of female C57BL/6J mice as previously reported [26]. Bone marrow cells were suspended in RPMI 1640 medium containing 2% NCS and carefully added onto 62% Percoll (GE Healthcare, Chicago, IL, USA) in RPMI 1640 medium.…”

ω3 fatty acid metabolite, 12‐hydroxyeicosapentaenoic acid, alleviates contact hypersensitivity by downregulation of CXCL1 and CXCL2 gene expression in keratinocytes via retinoid X receptor α

“…In addition to 17,18‐EpETE and 12‐HEPE, several other lipid mediators have been identified that inhibit CHS by targeting different cells. For example, oleic acid‐derived mead acid acts directly on neutrophils to inhibit their migration and leukotriene B 4 production, 41 and EPA‐derived RvE1, which is a metabolite of 18‐HEPE, impairs the mobility of cutaneous dendritic cells by blocking leukotriene B 4 ‐leukotriene B 4 receptor 1 signaling, thereby reducing skin inflammation in CHS 39 . However, although 18‐HEPE is a substrate of functional EPA‐derived metabolites of RvEs, we found here that 18‐HEPE had little effect on ear swelling, suggesting that 18‐HEPE is not metabolized to RvEs.…”