Hot new therapy for sepsis and the acute respiratory distress syndrome.

Abstract

In 1962 Ritossa demonstrated that exposing Drosophila to elevations of temperature produced “puffing” patterns of polytene chromosomes indicating increased gene expression (1). Five years later, Ashbaugh and colleagues described a new clinical syndrome, a form of non-cardiogenic pulmonary edema that they called the acute respiratory distress syndrome (ARDS) (2). These unrelated papers from widely disparate research areas pioneered independent research fields which are now intersecting, as demonstrated by the article by Weiss and colleagues in this issue of the JCI (3). This convergence of basic science with clinical research promises to influence the care of our most critically ill patients and offers an excellent model of how basic scientific discoveries, without any apparent clinical implications, can lead to novel therapies. Here, I will focus on the implications of these findings for possible new therapeutic options for ARDS, as well as on how this study provides new insights into the pathophysiology of sepsis/ARDS.