Around 2% of school children in the UK are allergic to peanuts. Severe eczema in early infancy has also been linked to food allergies, particularly peanut allergy.
A major break-through in our understanding of eczema has been made with the discovery of the FLG gene which codes for the skin barrier protein, filaggrin.
Mutations in the FLG gene result in an impaired skin barrier which is thought to allow allergens to penetrate the skin and sensitise the body.
The study, published this month in the Journal of Allergy and Clinical Immunology, was carried out in 557 children from the Manchester Asthma and Allergy Study (MAAS) – a flagship study from the University of Manchester and University Hospital of South Manchester led by Professors Adnan Custovic and Angela Simpson – who have been followed from birth (1996/7) to the present day.
The children in MAAS, who are representative of the normal population, have been thoroughly assessed for peanut allergy with skin prick tests, blood tests and in some cases oral food challenge tests and peanut allergy was diagnosed in 3% of them.
They have undergone genetic tests and 9% of them carry mutations in the FLG gene. In addition, dust samples were collected from their home environment in early life, in which it was possible to quantify peanut protein.
Peanut protein is present on hands and in saliva for up to three hours after peanuts or peanut-based food has been eaten, and can persist on table surfaces and sofa or pillow dust even after routine cleaning.
By combining information on genetics and the environment, it was possible to gain insights on risk factors for peanut allergy. For children who did not carry an FLG mutation, the amount of peanut protein in the house dust had no significant effect on whether or not the child developed peanut allergy.
For children with an FLG mutation, higher levels of peanut protein in household dust in infancy increased the likelihood of peanut allergy in childhood. For example, a three-fold increase in house dust peanut exposure during infancy was associated with a three-fold increase in risk of peanut allergy.
Professor Angela Simpson, from The University of Manchester’s Institute of Inflammation and Repair, said: “This is yet another example of how both genes and the environment are important in determining whether or not individuals develop allergic diseases. It is only because we were able to follow these children from before birth and take samples from their home environment in early life that it was possible to identify these effects.
“Gaining a better understanding of risk factors for diseases is the first step towards developing methods of prevention that are targeted to individuals at risk, which can be tested in clinical trials.”
Notes for editors
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‘Peanut allergy: Effect of environmental peanut exposure in children with filaggrin loss-of-function mutations’ by Brough et al is published in the Journal of Allergy and Clinical Immunology and can be accessed at http://dx.doi.org/10.1016/j.jaci.2014.08.011.
The Manchester Asthma and Allergy Study was supported by Medical Research Council grants, JP Moulton Charitable Foundation, North West Lung Centre Charity and National Institute for Health Research Clinical Research Facility at the University of South Manchester NHS Foundation Trust. The Centre for Dermatology and Genetic Medicine at the University of Dundee is supported by the Wellcome Trust.
The study was funded by Action Medical Research and supported by the National Institute for Health Research (NIHR) Clinical Research Facility at Guy’s & St. Thomas’ NHS Foundation Trust and the NIHR Biomedical Research Centre based at Guy’s and St Thomas’ NHS Foundation Trust and Kings College London.