Experimental and clinical data indicate that the inflammatory response after myocardial infarction (MI) is essential for adequate cardiac repair and that dysregulated/excessive inflammation promotes adverse remodeling and heart failure.
Recent high-parameter technologies such as single-cell RNA sequencing have enabled an encompassing analysis of the heart’s cellular composition after MI, including the identification of rare cell populations or distinct cellular subsets. Our attention was drawn to the presence of basophil granulocytes – an immune cell type classically associated with allergic responses and parasitic infections.
We identified a regulatory role of this cell type in the healing process after MI both in mice and in humans. Reduced basophil levels result in impaired left ventricular function post-MI and a pro-inflammatory cardiac micro-environment. Mechanistically, the findings could in large part be explained by basophil-specific secretion of the cytokines IL-4 and IL-13, which in turn facilitated differentiation and polarization of reparative macrophages in the healing heart.