Key to eczema’s itch uncovered

By Helen Albert, Senior medwireNews Reporter

An influx of neutrophils that secrete a lipid called leukotriene B4 (LTB4) is responsible for triggering the itching and inflammation of the skin typically seen in patients with eczema, suggest study findings.

The research is still at an early stage, but the team believes that blockade of this signaling cascade may help slow or halt the progression of eczema, a common skin condition affecting around 15% of children.

"Our findings suggest that neutrophils play a key role in allergic skin inflammation and that blockade of LTB4 and its receptor might provide a new therapy for eczema," commented lead author Michiko Oyoshi (Harvard University, Boston, Massachusetts, USA) in a press statement.

Oyoshi and co-investigators showed that tape stripping of mouse skin, to simulate itching, causes an influx of neutrophils to the surrounding area.

The first neutrophils in the irritated area of skin secrete LTB4, which triggers the arrival of more neutrophils through activation of the LTB4 receptor BLT1 on the neutrophil cell surface, as well as triggering an influx of T cells, that together make the skin more inflamed and irritated.

Mice that had neutrophils with nonfunctional BLT1 and that were deficient in the LTB4-synthesising enzyme LTA4H had a minimal inflammatory response to skin irritation triggered by tape stripping and application of ovalbumin. When wild type neutrophils were transferred to these mice the normal inflammatory response was re-instated.

The researchers found that they were able to block LTB4 synthesis and subsequent allergic skin response to mechanical stimuli in mice using pharmacologic agents.

Raif Geha, a co-author of the study, published in Immunity, and fellow Harvard University researcher, told the press: "We showed that a drug that blocks the production of leukotriene B4 blocks the development of allergic skin inflammation in a mouse model of eczema." They also found that blocking BLT1 receptors had a similar effect.

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