Less inflammation = better healing

This post was originally published on this site

by Bill Snyder

Myocardial infarction (MI), commonly called heart attack, remains a leading cause of mortality and morbidity worldwide, raising an urgent need for novel therapies.

Acute MI provokes an inflammatory response in the heart that removes damaged tissue to promote repair and regeneration. Overactive and/or prolonged inflammation impedes healing, however, suggesting that reducing inflammation may lead to better outcomes.

Previously Lan Wu, MD, Luc Van Kaer, PhD, and colleagues identified a subpopulation of regulatory B lymphocytes in the fat tissue of obese mice that secretes interleukin-10 (IL-10), an anti-inflammatory cytokine which protects against obesity-associated insulin resistance.

Reporting now in the Proceedings of the National Academy of Sciences, they found IL-10-producing B cells in mice also are highly enriched in fat tissue around the heart. Following MI, the cells increase in number and move to the damaged heart, where they terminate inflammation and protect against further injury and dysfunction.

IL-10-producing B cells thus are novel targets to improve the outcome of MI, the researchers concluded.

This research was supported by grants from the National Institutes of Health (DK081536, DK104817, HL133290, HL119234) and the American Heart Association.