TY - JOUR
AU - Sicklinger, Florian
AU - Meyer, Ingmar Sören
AU - Li, Xue
AU - Radtke, Daniel
AU - Dicks, Severin
AU - Kornadt, Moritz P
AU - Mertens, Christina
AU - Meier, Julia K
AU - Lavine, Kory J
AU - Zhang, Yunhang
AU - Kuhn, Tim Christian
AU - Terzer, Tobias
AU - Patel, Jyoti
AU - Börries, Melanie
AU - Schramm, Gabriele
AU - Frey, Norbert
AU - Katus, Hugo A
AU - Voehringer, David
AU - Leuschner, Florian
TI - Basophils balance healing after myocardial infarction via IL-4/IL-13.
JO - The journal of clinical investigation
VL - 131
IS - 13
SN - 1558-8238
CY - Ann Arbor, Mich.
PB - ASCJ
M1 - DKFZ-2021-01488
SP - e136778
PY - 2021
AB - The inflammatory response after myocardial infarction (MI) is a precisely regulated process that greatly affects subsequent remodeling. Here, we show that basophil granulocytes infiltrated infarcted murine hearts, with a peak occurring between days 3 and 7. Antibody-mediated and genetic depletion of basophils deteriorated cardiac function and resulted in enhanced scar thinning after MI. Mechanistically, we found that basophil depletion was associated with a shift from reparative Ly6Clo macrophages toward increased numbers of inflammatory Ly6Chi monocytes in the infarcted myocardium. Restoration of basophils in basophil-deficient mice by adoptive transfer reversed this proinflammatory phenotype. Cellular alterations in the absence of basophils were accompanied by lower cardiac levels of IL-4 and IL-13, two major cytokines secreted by basophils. Mice with basophil-specific IL-4/IL-13 deficiency exhibited a similarly altered myeloid response with an increased fraction of Ly6Chi monocytes and aggravated cardiac function after MI. In contrast, IL-4 induction in basophils via administration of the glycoprotein IPSE/α-1 led to improved post-MI healing. These results in mice were corroborated by the finding that initially low counts of blood basophils in patients with acute MI were associated with a worse cardiac outcome after 1 year, characterized by a larger scar size. In conclusion, we show that basophils promoted tissue repair after MI by increasing cardiac IL-4 and IL-13 levels.
KW - Cardiology (Other)
KW - Cardiovascular disease (Other)
KW - Heart failure (Other)
KW - Innate immunity (Other)
LB - PUB:(DE-HGF)16
C6 - pmid:34196299
DO - DOI:10.1172/JCI136778
UR - https://inrepo02.dkfz.de/record/169666
ER -