Systolic overload-induced pulmonary inflammation, fibrosis, oxidative stress and heart failure progression through interleukin-1 β

Chronic heart failure is associated with increased interleukin-1 β (IL-1β), leukocyte infiltration, and fibrosis in the heart and lungs. Here we further studied the role of IL-1β in the transition from left heart failure to pulmonary hypertension and right ventricular hypertrophy in mice with existing left heart failure produced by transverse aortic constricti on. We demonstrated that transverse aortic constriction-induced heart failure was associated with increased lung inflammation and cleaved IL-1β, and inhibition of IL-1β signaling using blocking antibodies of clone: B122 effectively attenuated further decrease of left ventricular systolic function in mice with existing heart failure.
Source: Journal of Molecular and Cellular Cardiology - Category: Cytology Authors: Source Type: research