Journal
CIRCULATION RESEARCH
Volume 114, Issue 4, Pages 637-649Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.114.302625
Keywords
adaptive immunity; inflammation; interleukin-10; killer cells; natural; myocardial infarction
Funding
- Japanese Science and Technology Agency
- Japan Society for the Promotion of Science [5556]
- China Scholarship Council [2008623017]
- Grants-in-Aid for Scientific Research [23390217] Funding Source: KAKEN
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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-, interleukin [IL]-6, and IL-1), 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--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-1-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.
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