title: Interleukin-13 deficiency aggravates healing and remodeling in male mice after experimental myocardial infarction.
abstract: BACKGROUND
  Activation of innate immunity, especially infiltration of monocytes, is critical for proper wound healing and scar formation after myocardial infarction (MI). Therefore, we tested the hypothesis that interleukin-13 (IL-13), which influences the differentiation of monocytes/macrophages and has profibrotic properties, modulates wound healing and remodeling after MI.
  
  
  RESULTS
  MI was induced by permanent ligation of the left coronary artery in both male and female wild-type (WT)/IL-13(-/-) mice. Real-time polymerase chain reaction demonstrated that expression of IL-13 was induced in left and right ventricular myocardium of WT mice within days in response to MI. Fifty-six-day survival was significantly impaired (65% in WT versus 34% in IL-13(-/-)) in male but not female IL-13(-/-) (55% in WT versus 54% in IL-13(-/-)) mice. Serial echocardiography showed significantly increased left ventricular dilation in male IL-13(-/-) compared with WT mice starting from day 1 after MI, despite comparable infarct size. Fluorescence-activated cell sorter analysis revealed less leukocyte infiltration in male IL-13(-/-) mice on day 3. Real-time polymerase chain reaction analysis demonstrated reduced expression of marker genes of alternative activation in monocytes sorted from the infarct zone of male IL-13(-/-) in comparison with WT mice on day 3 after MI.
  
  
  CONCLUSIONS
  Genetic deficiency of IL-13 worsens outcome after MI in male mice. Our data indicate that IL-13 regulates leukocyte recruitment and induces M2-like monocyte/macrophage differentiation, which modifies wound healing within the infarct zone.
authors: From the Department of Internal Medicine I, University Hospital Würzburg, Germany, and Comprehensive Heart Failure Center, University of Würzburg, Germany. hofmann_u2@klinik.uni-wuerzburg.de.
authors: Ulrich
authors: U
authors: Hofmann
authors: From the Department of Internal Medicine I, University Hospital Würzburg, Germany, and Comprehensive Heart Failure Center, University of Würzburg, Germany.
authors: Susanne
authors: S
authors: Knorr
authors: From the Department of Internal Medicine I, University Hospital Würzburg, Germany, and Comprehensive Heart Failure Center, University of Würzburg, Germany.
authors: Benjamin
authors: B
authors: Vogel
authors: From the Department of Internal Medicine I, University Hospital Würzburg, Germany, and Comprehensive Heart Failure Center, University of Würzburg, Germany.
authors: Johannes
authors: J
authors: Weirather
authors: From the Department of Internal Medicine I, University Hospital Würzburg, Germany, and Comprehensive Heart Failure Center, University of Würzburg, Germany.
authors: Anna
authors: A
authors: Frey
authors: From the Department of Internal Medicine I, University Hospital Würzburg, Germany, and Comprehensive Heart Failure Center, University of Würzburg, Germany.
authors: Georg
authors: G
authors: Ertl
authors: From the Department of Internal Medicine I, University Hospital Würzburg, Germany, and Comprehensive Heart Failure Center, University of Würzburg, Germany.
authors: Stefan
authors: S
authors: Frantz
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D004195:Disease Models, Animal; D004452:Echocardiography; D005260:Female; D005786:Gene Expression Regulation; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D018793:Interleukin-13 / Q000096:biosynthesis / Q000172:deficiency* / Q000235:genetics*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D009203:Myocardial Infarction / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D012313:RNA / Q000235:genetics*; D060888:Real-Time Polymerase Chain Reaction; D020257:Ventricular Remodeling / Q000235:genetics*
chemical_list: D018793:Interleukin-13; D012313:RNA
keywords: fibrosis; interleukin-13; monocytes; myocardial infarction; wound healing