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| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Meng, Qing-Lin Liu, Fei Yang, Xing-Yuan Liu, Xiao-Mei Zhang, Xia Zhang, Chun Zhang, Zong-De |
| Abstract | Background Latent tuberculosis infection (LTBI) relies on a homeostasis of macrophages and Mycobacterium tuberculosis (Mtb). The small heat shock protein, Mtb Hsp16.3 (also known as latency-associated antigen), plays an important role in Mtb persistence within macrophages. However, the mechanism of LTBI remains elusive. The aim of this study was to delineate LTBI-related miRNA expression in U937 macrophages expressing Mtb Hsp16.3 protein. U937 macrophages were infected with an integrase-deficient Lentivirus vector to transiently express Mtb Hsp16.3, and green fluorescent protein (GFP) as a control. We used a microRNA (miRNA) microarray chip containing more than 1000 probes to identify the significant differentially expressed miRNAs in the infected U937 cells, and employed real-time quantitative polymerase chain reaction (qRT-PCR) for validation. Furthermore, we confirmed these candidate LTBI-related miRNAs in peripheral blood mononuclear cells from subjects with LTBI and in healthy control individuals. Functional annotation prediction of miRNA target genes and pathway enrichment analyses were used to explore the putative links between these miRNAs and LTBI. Results Analysis of the miRNA expression profile identified 149 miRNAs that were differentially expressed in U937 macrophages expressing Mtb Hsp16.3 compared with the control expressing GFP. The expression level of seven miRNAs (miR-424-5p, miR-493-5p, miR-296-5p, miR-27b-3p, miR-377-5p, miR-3680-5p, miR-191-5p) were validated by qRT-PCR. The expression level of four miRNAs (miR-424-5p, miR-27b-3p, miR-377-5p, miR-3680-5p) in the peripheral blood mononuclear cells samples from LTBI and healthy participants reflected the altered patterns observed in the microarray profile. The bioinformatic analyses suggest that the miRNAs may regulate Mtb latent infection by affecting the development of macrophage cells. Conclusions The results suggest that miRNA expression may play a considerable role in the pathogenesis of LTBI, and this would increase our understanding of the molecular basis of Hsp16.3-facilitated Mtb survival in macrophages. |
| Related Links | https://bmcmicrobiol.biomedcentral.com/counter/pdf/10.1186/1471-2180-14-37.pdf |
| Ending Page | 9 |
| Page Count | 9 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| ISSN | 14712180 |
| DOI | 10.1186/1471-2180-14-37 |
| Journal | BMC Microbiology |
| Issue Number | 1 |
| Volume Number | 14 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2014-02-12 |
| Access Restriction | Open |
| Subject Keyword | Microbiology Biological Microscopy Mycology Parasitology Virology Life Sciences Mycobacterium Tuberculosis microRNAs Macrophages Small heat shock protein Latent tuberculosis infection |
| Content Type | Text |
| Resource Type | Article |
| Subject | Microbiology Microbiology (medical) |
| Journal Impact Factor | 4/2023 |
| 5-Year Journal Impact Factor | 4.6/2023 |
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