miR-223 is upregulated in monocytes from patients with tuberculosis and regulates function of monocyte-derived macrophages
| Autor: | Zhihong Cao, Bingfen Yang, Xiaoxing Cheng, Ruo Wang, Jing Jiang, Yanhua Liu |
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| Rok vydání: | 2015 |
| Předmět: |
Adult
Male Tuberculosis medicine.medical_treatment Interleukin-1beta Immunology Biology Monocytes Mycobacterium tuberculosis Downregulation and upregulation mir-223 medicine Humans RNA Messenger Phosphorylation Molecular Biology Cell Nucleus Regulation of gene expression U937 cell Interleukin-12 Subunit p40 Macrophages NF-kappa B biology.organism_classification medicine.disease NFKB1 Up-Regulation MicroRNAs Cytokine Gene Expression Regulation Case-Control Studies Leukocytes Mononuclear Female |
| Zdroj: | Molecular Immunology. 67:475-481 |
| ISSN: | 0161-5890 |
| DOI: | 10.1016/j.molimm.2015.08.006 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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