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Uric acid - a new look at an old marker of inflammation

29 July 2013

Scope 51

Changes in serum uric acid levels are a common feature of many human inflammatory diseases.

Recently there has been a significant escalation in inflammation-related conditions associated with the rise in obesity in developed countries. These conditions include type II diabetes, cardiovascular disease and gouty arthritis – commonly grouped under the term ‘metabolic syndrome’.

A common feature of metabolic syndrome is high levels of uric acid in the blood (hyperuricaemia), however, whether hyperuricaemia is the cause or effect of these inflammatory conditions remains to be determined.

Dr Jacquie Harper’s Arthritis & Inflammation team (pictured above) is looking at how both the crystalline and soluble forms of uric acid influence inflammation and immune cell function in both clinical and basic research settings.

Collectively these studies are providing important insights into new potential therapeutic options for the improved management of inflammatory diseases.

Gouty arthritis – a clinical perspective

Gout is an intensely painful form of arthritis affecting many New Zealanders. A gout attack is triggered when uric acid crystallises in the joints, causing rapid and painful joint inflammation. Previous research from Dr Harper’s team, collaborating with Wellington Rheumatologists Prof Andrew Harrison and Dr Rebecca Grainger, showed that high serum uric acid levels may moderate the inflammatory response to the crystals. To determine how this happens, PhD student Rene McLaughlin is working on a clinical study involving gout patients, collaborating with Christchurch Rheumatologist Assoc Prof Lisa Stamp and Professor Tony Kettle.

Neutrophil cannibalism and gout

Neutrophils are one of the first inflammatory cells to respond to the uric acid crystals that trigger inflammation in gout. Previously thought to be primarily responsible for driving gout attacks, PhD student Stefanie Steiger has now shown that neutrophils could also be part of a cure – once they start ‘eating’ each other that is! On contact with gout crystals, neutrophils release reactive oxygen species, and then die off. The dead neutrophils are then cleared by other neutrophils. This triggers the cells to produce a protein called TGF-?1, which shuts down inflammation. Dr Harper’s team is now exploring different ways to target neutrophil ‘cannibalism’ in the joints, so they can switch off inflammation at the very early stages of a gout attack.


While high serum uric acid levels are a primary risk factor for developing gout, they are also observed in diseases of the metabolic syndrome such as obesity. Research to date has focused on the inflammatory environment in adipose (fat) tissue and there is little information available on how diet-driven obesity affects other immune cell populations. To address this question, Dr Odette Shaw, in collaboration with Auckland Rheumatologist Assoc Prof Nicola Dalbeth, has been investigating how hyperuricaemia alters the inflammatory immune responses of obese and non-obese mice. Her research confirms that obesity does indeed raise the background level of inflammation in non-adipose tissues, but that it does not appear to exacerbate gouty arthritis.

Image caption: Rene McLaughlin, Stefanie Steiger, Dr Odette Shaw, Dr Jacquie Harper, Lisa Shaw.

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