Role of cardiac- and myeloid-MyD88 signaling in endotoxin shock: a study with tissue-specific deletion models.

ABSTRACT:

Background

Myeloid differentiation factor 88 (MyD88) is an adaptor molecule critical for host innate immunity. Studies have shown that signaling via MyD88 contributes to cytokine storm, cardiac dysfunction, and high mortality during endotoxin shock.However, the specific contribution of MyD88 signaling of immune and cardiac origins to endotoxin shock remains unknown.

Methods

Tissue-specific MyD88 deletion models: Cre-recombinase transgenic mice with α-myosin heavy chain (α-MHC) or lysozyme M promoters were cross-bred with MyD88-loxP (MyD88fl/fl) mice, respectively, to generate cardiomyocyte- (α-MHCMyD88−/−) or myeloid-specific (Lyz-MyD88−/−) MyD88 deletion models and their respective MyD88fl/fl littermates. Endotoxin shock model: Mice were subjected to 15 mg/kg lipopolysaccha

SUBMITTER: Feng Y 

PROVIDER: S-EPMC4237623 | biostudies-literature | 2014 Dec

REPOSITORIES: biostudies-literature