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Mol Immunol. 2015 Oct;67(2 Pt B):475-81. doi: 10.1016/j.molimm.2015.08.006. Epub 2015 Aug 18.

miR-223 is upregulated in monocytes from patients with tuberculosis and regulates function of monocyte-derived macrophages.

Author information

1
Key Laboratory of Tuberculosis Prevention and Treatment, Beijing Key Laboratory of New Techniques for Tuberculosis Diagnosis and Treatment, Institute of Tuberculosis, 309th Hospital, Beijing, China.
2
Key Laboratory of Tuberculosis Prevention and Treatment, Beijing Key Laboratory of New Techniques for Tuberculosis Diagnosis and Treatment, Institute of Tuberculosis, 309th Hospital, Beijing, China. Electronic address: xcheng2@139.com.

Abstract

Tuberculosis (TB) is a serious infectious disease that most commonly affects the lungs. Macrophages are among the first line defenders against establishment of Mycobacterium tuberculosis infection in the lungs. In this study, we found that activation and cytokine production in monocyte-derived macrophages (MDM) from patients with active TB was impaired. miR-223 expression was significantly elevated in monocytes and MDM from patients with TB compared with healthy controls. To determine the functional role of miR-223 in macrophages, stable miR-223-expressing and miR-223 antisense-expressing U937 cells were established. Compared with empty vector controls, expression of IL-1β, IL-6, TNF-α and IL-12p40 genes was significantly higher in miR-223 antisense-expressing U937 cells, but lower in miR-223-expressing U937 cells. miR-223 can negatively regulate activation of NF-κB by inhibition of p65 phosphorylation and nuclear translocation. It is concluded that miR-223 can regulate macrophage function by inhibition of cytokine production and NF-κB activation.

KEYWORDS:

Macrophages; Tuberculosis; microRNA-223

PMID:
26296289
DOI:
10.1016/j.molimm.2015.08.006
[Indexed for MEDLINE]

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