Feeding of a fat-enriched diet causes the loss of resistance to contact hypersensitivity

Background Low-molecular weight chemicals or metal ions can cause allergic contact dermatitis, an inflammatory skin disease. Mice lacking Toll-like receptors 2 and 4 (TLR2/4 mice) are resistant to contact hypersensitivity (CHS). In the Western population obesity is increasing, which is known to have a proinflammatory impact. Objectives The aim of this study was to investigate the impact of a high-fat diet (HFD) on the sensitization and elicitation of CHS. We hypothesized that a proinflammatory micromilieu can be caused by an increase in adipose tissue, which might be sufficient to break the resistance of TLR2/4 mice. Methods Four weeks prior to sensitization, wild-type (wt) or TLR2/4 mice were fed normal chow (NC), control diet (CD), or HFD. The effects on CHS and inflammation were analysed by measuring the ear swelling response, using flow cytometry and enzyme-linked immunosorbent assay. Results The reaction of wt mice to 2,4,6-trinitro-1-chlorobenzene (TNCB) was increased by HFD. While NC-fed TLR2/4 mice were still resistant to CHS, HFD and, unexpectedly, CD feeding broke the resistance of TLR2/4 mice to TNCB. Conclusions These experiments suggest that the increased fat content or the different fatty acid composition of the diets increases inflammation and, therefore, the likelihood of developing CHS.

Automated summary

This study found that a high-fat diet may increase sensitization and elicitation of allergic contact dermatitis (CHS), particularly impacting the resistance of mice lacking Toll-like receptors 2 and 4.