| First Author | Yan X | Year | 2014 |
| Journal | Circ Res | Volume | 114 |
| Issue | 4 | Pages | 637-49 |
| PubMed ID | 24366170 | Mgi Jnum | J:223700 |
| Mgi Id | MGI:5660087 | Doi | 10.1161/CIRCRESAHA.114.302625 |
| Citation | Yan X, et al. (2014) Lung natural killer cells play a major counter-regulatory role in pulmonary vascular hyperpermeability after myocardial infarction. Circ Res 114(4):637-49 |
| abstractText | RATIONALE: Natural killer (NK) cells are lymphocytes of the innate immune system that play specialized and niche-specific roles in distinct organs. OBJECTIVE: We investigated the possible function of NK cells in the pathogenesis of congestive heart failure after myocardial infarction. METHODS AND RESULTS: Depletion of NK cells from mice had little effect on cytokine expression (tumor necrosis factor-alpha, interleukin [IL]-6, and IL-1beta), neutrophil and macrophage infiltration into infarcted myocardium, or left ventricular remodeling after myocardial infarction. However, these mice exhibited severe respiratory distress associated with protein-rich, high-permeability alveolar edema accompanied by neutrophil infiltration. In addition, there were 20-fold more NK cells in the mouse lungs than in heart, and these cells were accumulated around the vasculature. CD107a-positive and interferon-gamma-positive cell populations were unchanged, whereas IL-10-positive populations increased. Adoptive transfer of NK cells from wild-type mice, but not from IL-10 knockout mice, into the NK cell-depleted mice rescued the respiratory phenotype. IL-1beta-mediated dextran leakage from a lung endothelial cell monolayer was also blocked by coculture with NK cells from wild-type mice but not from IL-10 knockout mice. CONCLUSIONS: This study is the first to identify a critical role for lung NK cells in protecting lung from the development of cardiogenic pulmonary edema after myocardial infarction. |
