Science News

... from universities, journals, and other research organizations

Discovery Improves Understanding of Early Onset Inflammatory Disease

July 5, 2012 — Scientists at the University of East Anglia (UEA) have discovered a 'constant cloud' of potent inflammatory molecules surrounding the cells responsible for diseases such as thickening of the arteries and rheumatoid arthritis.


Share This:

Published online recently by The Journal of Cell Science, the findings could eventually lead to new treatments for chronic inflammatory diseases. Cardiovascular disease arising from atherosclerosis (thickening of the arteries) kills around 17 million people worldwide each year, including 120,000 people in England and Wales, while rheumatoid arthritis affects around 400,000 people in the UK.

The UEA team studied a type of white blood cell called monocytes. Monocytes play an important role in the human immune system and help protect our bodies against infection. But they can also invade tissue, triggering the early stages of common inflammatory diseases.

The researchers detected for the first time that monocytes were surrounded by a constant cloud. This cloud was found to be made up of potent inflammatory molecules called adenosine triphosphate, or ATP. Further study showed that the ATP molecules were being propelled through the cell wall by the actions of lysosomes. Lysosomes are sub-cellular compartments within blood cells which had previously been thought to only break down cell waste.

"These unexpected findings shed light on the very early stages in the development of inflammatory diseases such as atherosclerosis and rheumatoid arthritis," said lead author Dr Samuel Fountain of UEA's School of Biological Sciences.

"We found that lysosomes are actually highly dynamic and play a key role in the way inflammatory cells function. This is an exciting development that we hope will lead to the discovery of new targets for inflammatory drugs in around five years and potential new treatments beyond that."

Dr Fountain said further study was now needed to investigate how to control the release of ATP by lysosomes in monocytes and other white blood cells, and to understand how inflammation may be affected in patients with inherited diseases involving lysosomes.

Dr Fountain is a Biotechnology and Biological Sciences Research Council (BBSRC) David Phillips Fellow and recently received £0.9m from the BBSRC to study how cells use ATP as a signalling molecule.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

|

Story Source:

The above story is reprinted from materials provided by University of East Anglia.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Venketesh Sivaramakrishnan, Stefan Bidula, Hinnah Campwala, Divya Katikaneni, and Samuel J. Fountain. Constitutive lysosome exocytosis releases ATP and engages P2Y receptors in human monocytes. The Journal of Cell Science, July 5, 2012 DOI: 10.1242/jcs.107318
APA

MLA

Note: If no author is given, the source is cited instead.

Search ScienceDaily

Number of stories in archives: 137,193

Find with keyword(s):
 
Enter a keyword or phrase to search ScienceDaily's archives for related news topics,
the latest news stories, reference articles, science videos, images, and books.

Recommend ScienceDaily on Facebook, Twitter, and Google:

Other social bookmarking and sharing services:

|

 
  more breaking science news

Social Networks


Recommend ScienceDaily on Facebook, Twitter, and Google +1:

Other social bookmarking and sharing tools:

|

Breaking News

... from NewsDaily.com

In Other News ...

Science Video News


Identical Twins Identical Problems

A University of Michigan Medical School rheumatologist and his colleagues are beginning to comprehend how identical twins can be so different when it. ...  > full story

Strange Science News

 

Free Subscriptions

... from ScienceDaily

Get the latest science news with our free email newsletters, updated daily and weekly. Or view hourly updated newsfeeds in your RSS reader:

Feedback

... we want to hear from you!

Tell us what you think of ScienceDaily -- we welcome both positive and negative comments. Have any problems using the site? Questions?

Post this page to your favorite social bookmarking site:
Include this item in your blog or web site:
Cite this article in your essay, paper, or report:
Email this page's link to a friend or colleague: