The identified miRNAs were predicted to modulate 7044 target genes. We then used the NCBI DAVID server to identify

the significantly enriched pathways involving the predicted target genes. As shown in Table  3, apart from cancer-associated pathways, the MAPK signaling, endocytosis, Wnt signaling, focal adhesion, axon guidance, and TGF-beta signaling pathways, which are related to differentiation, polarization, and versatility of macrophages, were significantly enriched. The results suggest that the miRNAs may regulate Mtb infection by affecting the development of immune cells. Table 3 Enriched pathways involving the predicted target genes Pathway name p value Pathways in cancer 5.60E-16 MAPK signaling pathway 1.70E-14 Endocytosis 6.90E-14 Neurotrophin signaling pathway 1.50E-13 Wnt signaling Selleck Emricasan XAV-939 solubility dmso pathway 6.50E-13 Focal adhesion

7.60E-11 Axon guidance 1.10E-10 ErbB signaling pathway 7.10E-09 Glioma 5.80E-08 Basal cell carcinoma 6.20E-08 Long-term potentiation 6.30E-08 TGF-beta signaling pathway 9.10E-08 Regulation of actin cytoskeleton 1.10E-07 mTOR signaling pathway 3.PD-1/PD-L1 activation 70E-07 Adherens junction 1.30E-06 Chemokine signaling pathway 1.10E-05 Long-term depression 1.90E-05 T cell receptor signaling pathway 3.00E-05 Gap junction 5.60E-05 Fc gamma R-mediated phagocytosis 1.60E-04 B cell receptor signaling pathway 4.60E-04 GnRH signaling pathway 5.40E-04 Fc epsilon RI signaling pathway 7.60E-04 Phosphatidylinositol signaling system 1.50E-03 VEGF signaling pathway 1.50E-03 Vascular smooth muscle contraction 2.20E-03 SNARE interactions in vesicular transport 2.40E-03 ECM-receptor interaction 2.40E-03 Discussion The macrophage is the main replication niche of Mtb, despite the selleck chemical bactericidal

characteristics and functions that this cell type normally has. The Mtb has evolved several strategies to reside and even replicate within the otherwise hostile environment of the macrophage, including the prevention of phagosome-lysosome fusion, inhibition of phagosomal maturation, and detoxification of the host’s stresses. Accordingly, the localization of Mtb inside the macrophage has been a matter of debate in recent years [13]. For a long time, an impermeable phagosome in the macrophage was thought to contain Mtb. However, recent evidence indicates that Mtb, as well as M. leprae, can escape its vacuole and reside in the host cell cytosol [14]. It is becoming clear that LTBI is not a static state with a homogenous population of non-replicating bacilli, but a constant endogenous Mtb reinfection process [15]. It is argued that both phagosomal maturation inhibition and escape from the phagosome are part of the survival strategies of Mtb.