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| 001 | 169666 | ||
| 005 | 20240312141419.0 | ||
| 024 | 7 | _ | |a 10.1172/JCI136778 |2 doi |
| 024 | 7 | _ | |a pmid:34196299 |2 pmid |
| 024 | 7 | _ | |a 0021-9738 |2 ISSN |
| 024 | 7 | _ | |a 1558-8238 |2 ISSN |
| 024 | 7 | _ | |a altmetric:108567364 |2 altmetric |
| 037 | _ | _ | |a DKFZ-2021-01488 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Sicklinger, Florian |b 0 |
| 245 | _ | _ | |a Basophils balance healing after myocardial infarction via IL-4/IL-13. |
| 260 | _ | _ | |a Ann Arbor, Mich. |c 2021 |b ASCJ |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1710249234_32557 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a 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. |
| 536 | _ | _ | |a 313 - Krebsrisikofaktoren und Prävention (POF4-313) |0 G:(DE-HGF)POF4-313 |c POF4-313 |f POF IV |x 0 |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, , Journals: inrepo01.inet.dkfz-heidelberg.de |
| 650 | _ | 7 | |a Cardiology |2 Other |
| 650 | _ | 7 | |a Cardiovascular disease |2 Other |
| 650 | _ | 7 | |a Heart failure |2 Other |
| 650 | _ | 7 | |a Innate immunity |2 Other |
| 700 | 1 | _ | |a Meyer, Ingmar Sören |b 1 |
| 700 | 1 | _ | |a Li, Xue |b 2 |
| 700 | 1 | _ | |a Radtke, Daniel |b 3 |
| 700 | 1 | _ | |a Dicks, Severin |b 4 |
| 700 | 1 | _ | |a Kornadt, Moritz P |b 5 |
| 700 | 1 | _ | |a Mertens, Christina |b 6 |
| 700 | 1 | _ | |a Meier, Julia K |b 7 |
| 700 | 1 | _ | |a Lavine, Kory J |b 8 |
| 700 | 1 | _ | |a Zhang, Yunhang |b 9 |
| 700 | 1 | _ | |a Kuhn, Tim Christian |b 10 |
| 700 | 1 | _ | |a Terzer, Tobias |0 P:(DE-He78)9c4af0f5ceb3a2072b3736274eadf20e |b 11 |
| 700 | 1 | _ | |a Patel, Jyoti |b 12 |
| 700 | 1 | _ | |a Börries, Melanie |0 P:(DE-He78)49bdb7cb4094fbf35c269ffa3e93ebc6 |b 13 |u dkfz |
| 700 | 1 | _ | |a Schramm, Gabriele |b 14 |
| 700 | 1 | _ | |a Frey, Norbert |b 15 |
| 700 | 1 | _ | |a Katus, Hugo A |b 16 |
| 700 | 1 | _ | |a Voehringer, David |b 17 |
| 700 | 1 | _ | |a Leuschner, Florian |b 18 |
| 773 | _ | _ | |a 10.1172/JCI136778 |g Vol. 131, no. 13, p. e136778 |0 PERI:(DE-600)2018375-6 |n 13 |p e136778 |t The journal of clinical investigation |v 131 |y 2021 |x 1558-8238 |
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| 914 | 1 | _ | |y 2021 |
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