White blood cell research shows how causing and conquering inflammation are inextricably linked

August 18, 2014
Aspirin, take 2
Scanning electron micrograph shows a macrophage. Credit: Image courtesy of National Cancer Institute.

Hugely popular non-steroidal anti-inflammation drugs like aspirin, naproxen (marketed as Aleve) and ibuprofen (Advil, Motrin) all work by inhibiting or killing an enzyme called cyclooxygenase – a key catalyst in production of hormone-like lipid compounds called prostaglandins that are linked to a variety of ailments, from headaches and arthritis to menstrual cramps and wound sepsis.

In a new paper, published this week in the online early edition of PNAS, researchers at the University of California, San Diego School of Medicine conclude that aspirin has a second effect: Not only does it kill cyclooxygenase, thus preventing production of the prostaglandins that cause and pain, it also prompts the enzyme to generate another compound that hastens the end of inflammation, returning the affected cells to homeostatic health.

"Aspirin causes the to make a small amount of a related product called 15-HETE," said senior author Edward A. Dennis, PhD, Distinguished Professor of Pharmacology, Chemistry and Biochemistry. "During infection and inflammation, the 15-HETE can be converted by a second enzyme into lipoxin, which is known to help reverse inflammation and cause its resolution – a good thing."

Specifically, Dennis and colleagues looked at the function of a type of called macrophages, a major player in the body's immune response to injury and infection. They found that macrophages contain the biochemical tools to not just initiate inflammation, a natural part of the immune response, but also to promote recovery from inflammation by releasing 15-HETE and converting it into lipoxin as the inflammation progresses.

Dennis said the findings may open new possibilities for anti-inflammatory therapies by developing new drugs based on analogues of lipoxin and other related molecules that promote resolution of inflammation. "If we can find ways to promote more resolution of inflammation, we can promote health," he said.

Explore further: Scientists discover molecule that does double duty in stopping asthma attacks

More information: Phospholipase A2 regulates eicosanoid class switching during inflammasome activation, PNAS, www.pnas.org/cgi/doi/10.1073/pnas.1404372111

Related Stories

Chronic inflammation accelerates ageing

June 25, 2014

(Medical Xpress)—Inflammation could be a key factor in the ageing process academics at Newcastle University have found, and the discovery could help scientists identify new ways of delaying ageing.

Recommended for you

Formaldehyde damages proteins, not just DNA

September 29, 2016

The capacity of formaldehyde, a chemical frequently used in manufactured goods such as automotive parts and wood products, to damage DNA, interfere with cell replication and cause cancer inspired new federal regulations this ...

Synthetic 3D-printed material helps bones regrow

September 28, 2016

A cheap and easy to make synthetic bone material has been shown to stimulate new bone growth when implanted in the spines of rats and a monkey's skull, researchers said Wednesday.

Epigenetic clock predicts life expectancy

September 28, 2016

UCLA geneticist Steve Horvath led a team of 65 scientists in seven countries to record age-related changes to human DNA, calculate biological age and estimate a person's lifespan. A higher biological age—regardless of chronological ...

Engineered blood vessels grow in lambs

September 27, 2016

In a hopeful development for children born with congenital heart defects, scientists said Tuesday they had built artificial blood vessels which grew unaided when implanted into lambs, right into adulthood.

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.