Gadolinium-based compounds induce NLRP3-dependent IL-1β production and peritoneal inflammation.

ABSTRACT:

Objective

Nephrogenic systemic fibrosis (NSF) is a progressive fibrosing disorder that may develop in patients with chronic kidney disease after administration of gadolinium (Gd)-based contrast agents (GBCAs). In the setting of impaired renal clearance of GBCAs, Gd deposits in various tissues and fibrosis subsequently develops. However, the precise mechanism by which fibrosis occurs in NSF is incompletely understood. Because other profibrotic agents, such as silica or asbestos, activate the nucleotide-binding oligomerisation domain (NOD)-like receptor protein 3 (NLRP3) inflammasome and initiate interleukin (IL)-1β release with the subsequent development of fibrosis, we evaluated the effects of GBCAs on inflammasome activation.

Methods

Bone marrow derived macrophages from C57

SUBMITTER: Schmidt-Lauber C 

PROVIDER: S-EPMC4428954 | biostudies-literature | 2015 Nov

REPOSITORIES: biostudies-literature