Anaphylaxis is a severe allergic reaction that is life threatening because it affects the function of multiple organ systems, including the lungs and blood vessels. Its effects on the latter cause them to widen, leading to a dramatic drop in blood pressure, a condition known as anaphylactic shock.
New research in mice, performed by Ana Olivera, Juan Rivera, and colleagues, at the National Institutes of Health, Bethesda, has identified a potential new drug target to counteract the widening of blood vessels that is associated with anaphylactic shock.
The proteins SphK1 and SphK2 are involved in generating the soluble molecule S1P, which has effects on blood vessels and the immune system via a family of proteins (S1PR1-S1PR5). In the study, mice lacking SphK2 were found to recover more rapidly from anaphylaxis than normal mice while mice lacking SphK1 recovered poorly. Treating mice lacking SphK1 with S1P dramatically improved their recovery.
As these effects of S1P were found to be mediated via S1PR2, the authors suggest that drugs that trigger S1PR2 might counteract the widening of blood vessels associated with anaphylactic shock, thereby promoting recovery.
The research appears in the Journal of Clinical Investigation.
- Ana Olivera, Christoph Eisner, Yoshiaki Kitamura, Sandra Dillahunt, Laura Allende, Galina Tuymetova, Wendy Watford, Francoise Meylan, Susanne C. Diesner, Lingli Li, Jurgen Schnermann, Richard L. Proia and Juan Rivera. Sphingosine kinase 1 and sphingosine-1-phosphate receptor 2 are vital to recovery from anaphylactic shock in mice. Journal of Clinical Investigation, 2010; DOI: 10.1172/JCI40659
Cite This Page: