The common view is that inflammation promotes the development of heart disease – we’ve shown that the truth is clearly more complicated.
- Daniel Freitag
The finding is one of the outcomes of research using a powerful new genetic tool that mimics the behaviour of certain anti-inflammatory drugs. The technique allows researchers to study the effects of inhibiting interleukin-1, a master regulator of inflammation, on a range of different outcomes not yet investigated in clinical trials.
Interleukin-1 plays a central role in regulating the body’s inflammatory response, setting off a cascade of signals within the body against infection and other damage. Certain drugs, such as anakinra, reduce inflammation by blocking interleukin-1. This action also occurs naturally in individuals who carry particular genetic variants.
Although inflammation is meant to be protective, a disproportionate response can be damaging to the body – for example, causing potentially life-threatening symptoms seen in severe cases of influenza infection. It also plays a crucial role in a number of autoimmune diseases such as rheumatoid arthritis. Although scientists suspected that it would also be likely to increase risk of cardiovascular disease, until now little evidence existed to confirm or disprove this suggestion.
To examine the long-term implications of blocking this pathway, researchers from the Interleukin-1 Genetics Consortium developed a ‘genetic score’ to combine the effects of two of these natural genetic variants. They looked at the effect of this score on key biological indicators of inflammation, comparing it to the effect of anakinra. They investigated this score in relation to several medical conditions including rheumatoid arthritis and coronary heart disease by analysing data from over a million individuals.
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Image:Heart pulse
Credit: Gabriela Pinto
Reproduced courtesy of the University of Cambridge
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