Role of G-protein-coupled adenosine receptors in downregulation of inflammation and protection from tissue damage

Akio Ohta and Michail Sitkovsky ()
Additional contact information
Akio Ohta: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Michail Sitkovsky: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health

Nature, 2001, vol. 414, issue 6866, 916-920

Abstract: Abstract Inappropriate or prolonged inflammation is the main cause of many diseases1; for this reason it is important to understand the physiological mechanisms that terminate inflammation in vivo2. Agonists for several Gs-protein-coupled receptors3, including cell-surface adenosine purinergic receptors4,5,6,7, can increase levels of immunosuppressive cyclic AMP in immune cells8,9,10,11,12,13,14,15; however, it was unknown whether any of these receptors regulates inflammation in vivo. Here we show that A2a adenosine receptors have a non-redundant role in the attenuation of inflammation and tissue damage in vivo. Sub-threshold doses of an inflammatory stimulus16,17 that caused minimal tissue damage in wild-type mice were sufficient to induce extensive tissue damage, more prolonged and higher levels of pro-inflammatory cytokines, and death of male animals deficient in the A2a adenosine receptor. Similar observations were made in studies of three different models of inflammation and liver damage as well as during bacterial endotoxin-induced septic shock. We suggest that A2a adenosine receptors are a critical part of the physiological negative feedback mechanism for limitation and termination of both tissue-specific and systemic inflammatory responses.

Date: 2001
References: Add references at CitEc
Citations: View citations in EconPapers (2)

Downloads: (external link)
https://www.nature.com/articles/414916a Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:414:y:2001:i:6866:d:10.1038_414916a

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/414916a

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().