Discovery can reduce the severity of allergic reactions and save lives
August 3, 2009
A new method to reducing the impact or symptoms of anaphylactic shock has been identified by researchers from Glasgow University (Scotland)
Source: University of Glasgow News
A team of researchers from Glasgow University are the first in the world to pinpoint a molecule which amplifies the allergic reaction and have successfully developed a biological agent to reduce the symptoms. The breakthrough could lead to a huge reduction in the number of fatal cases of anaphylactic shock across the world.
Anaphylaxis is a severe allergic reaction – the extreme end of the allergic spectrum. Symptoms may include generalised flushing, difficulty in breathing and can result in cardiac arrest and death.
Common causes of anaphylaxis include foods such as peanuts, tree nuts, sesame, fish, shellfish, dairy products and eggs. Non-food causes include wasp or bee stings, natural latex (rubber), penicillin or any other drug or injection.
Led by Dr Alirio Melendez and Prof Eddy Liew, both of the University of Glasgow, the team found that the novel cytokine (immune hormone) – IL-33 – plays a key role in the development of anaphylaxis. Dr Melendez said: “An anaphylactic shock prompts a massive inflammatory reaction which often is so severe that it constricts breathing. In our study we found that the severity of the shock is linked to the IL-33 molecule, which acts as an amplifier to the inflammatory reaction. This can lead to a fatal constriction of the airway and, ultimately, death.” “Our study suggests that patients with the most severe anaphylactic reactions have very high levels of IL33 in their system”. “In basic terms, without the IL33 molecule, the allergic reaction experienced would be far less severe, greatly reducing the risk of death.”
The findings have been published in the highly respected international journal, Proceedings of the National Association of Sciences of the USA (PNAS). The team successfully used a mouse model to show that blocking the IL-33 molecule reduces the severity of the attack. “This approach does not stop the allergic reaction altogether. It blocks the amplification of the reaction triggered by IL-33, not the allergic response itself.”. “Our current strategy is to utilise the soluble receptor for IL-33 (sST2) to validate as a potential biological agent that can potentially be used to target IL-33 during an anaphylactic shock”.
Lynne Regent, Chief Executive of The Anaphylaxis Campaign (UK), said: “The results of the study, led by Dr Melendez and Prof. Liew at The University of Glasgow, are encouraging. We would hope to see this work developed further to a point where it could be of real benefit to people living with Anaphylaxis or at risk of severe allergic reaction”.
For more information, contact Eleanor Cowie in the University of Glasgow Media Relations Office on 0141 330 3683 or email e.cowie@admin.gla.ac.uk
The cytokine interleukin-33 mediates anaphylactic shock. Pushparaj PN, Tay HK, H’ng SC, Pitman N, Xu D, McKenzie A, Liew FY, Melendez AJ. Proc Natl Acad Sci U S A. 2009 Jun 16;106(24):9773-8. Epub 2009 Jun 8.
University of Glasgow
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