4.5 Article

Dysregulation in microRNA expression in peripheral blood mononuclear cells of sepsis patients is associated with immunopathology

期刊

CYTOKINE
卷 71, 期 1, 页码 89-100

出版社

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2014.09.003

关键词

Cytokine; miRNA; Monocyte; Sepsis; miR-146a

资金

  1. National Institute of Health [R01 MH094755, P01 AT003961, P20 GM103641, R01 AT006888, R01 ES019313]
  2. Veterans Administration Merit Award [BX001357]
  3. National Center for Complementary & Integrative Health [R01AT006888, P01AT003961] Funding Source: NIH RePORTER
  4. NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES019313] Funding Source: NIH RePORTER
  5. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P20GM103641] Funding Source: NIH RePORTER
  6. NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH094755] Funding Source: NIH RePORTER
  7. Veterans Affairs [I01BX001357] Funding Source: NIH RePORTER

向作者/读者索取更多资源

Sepsis is a major cause of death worldwide. It triggers systemic inflammation, the role of which remains unclear. In the current study, we investigated the induction of microRNA (miRNA) during sepsis and their role in the regulation of inflammation. Patients, on days 1 and 5 following sepsis diagnosis, had reduced T cells but elevated monocytes. Plasma levels of IL-6, IL-8, IL-10 and MCP-1 dramatically increased in sepsis patients on day 1. T cells from sepsis patients differentiated primarily into Th2 cells, whereas regulatory T cells decreased. Analysis of 1163 miRNAs from PBMCs revealed that miR-182, miR-143, miR-145, miR-146a, miR-150, and miR-155 were dysregulated in sepsis patients. miR-146a downregulation correlated with increased IL-6 expression and monocyte proliferation. Bioinformatics analysis uncovered the immunological associations of dysregulated miRNAs with clinical disease. The current study demonstrates that miRNA dysregulation correlates with clinical manifestations and inflammation, and therefore remains a potential therapeutic target against sepsis. (C) 2014 Elsevier Ltd. All rights reserved.

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