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.