A Common Inflammatory Pathway In Silicosis And Alzheimer's

Many structurally diverse molecules, including bacterial toxins and various crystals such as silicon dioxide that cause silicosis in the lungs, induce inflammation by activating a protein complex inside cells called the inflammasome. Groups led by Eicke Latz and Douglas Golenbock show that silicon dioxide crystals and the form of beta-amyloid protein linked to Alzheimer's disease are taken up by cells in a way that produces inflammation. This process involves seepage of the cathepsin B protein from compartments called lysosomes, which destroy cellular debris. The release of cathepsin B triggers the uncontrolled immune responses associated with silicosis and Alzheimer's disease.

Characterizing this signalling cascade, which is very likely to be associated with other inflammatory diseases such as gout, may thus provide a common target for treatment of a myriad of conditions.

Author contacts:

Eicke Latz (University of Massachusetts Medical School, Worcester, MA, USA)
E-mail: eicke.latz@umassmed.edu

Douglas Golenbock (University of Massachusetts Medical School, Worcester, MA, USA)
E-mail: douglas.golenbock@umassmed.edu

Abstracts available online:
Abstract 1.
Abstract 2

(C) Nature Immunology press release.

Message posted by: Trevor M. D'Souza