A common inflammatory pathway in silicosis and Alzheimer’s

Two different chemical agents, one associated with Alzheimer’s, the other with a severe lung disease, cause inflammation in the same way, reports two studies published online this week in Nature Immunology. This finding could provide a therapeutic target for the treatment of these diseases.

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.