Modulation of the phosphoinositide 3-kinase signaling pathway alters host response to sepsis, inflammation, and ischemia/reperfusion injury

Shock. 2006 May;25(5):432-9. doi: 10.1097/01.shk.0000209542.76305.55.

Abstract

The phosphoinositide 3-kinases (PI3Ks) are a conserved family of signal transduction enzymes that are involved in regulating cellular activation, inflammatory responses, chemotaxis, and apoptosis. We have discovered that a carbohydrate ligand, glucan, will stimulate the endogenous PI3K/Akt signaling pathway. This article reviews the current data on the role of the PI3K/Akt signaling pathway as a negative feedback mechanism or compensatory regulator of septic and inflammatory responses. Of greater importance, the data reviewed in this article suggest that modulation of the PI3K/Akt signaling pathway can reduce the morbidity and mortality associated with septic and I/R injury. Thus, manipulation of the endogenous PI3K/Akt signaling pathway may represent a new and novel therapeutic approach to management of important diseases.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cytokines / metabolism
  • Glucans / chemistry
  • Humans
  • Immunity, Innate
  • Inflammation / enzymology*
  • Models, Biological
  • Myocardium / pathology
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Reperfusion Injury / enzymology*
  • Sepsis / enzymology*
  • Signal Transduction*
  • Time Factors
  • Toll-Like Receptor 4 / metabolism

Substances

  • Cytokines
  • Glucans
  • TLR4 protein, human
  • Toll-Like Receptor 4
  • Phosphatidylinositol 3-Kinases