Exosomal RNA from Mycobacterium tuberculosis-Infected Cells Is Functional in Recipient Macrophages.

Exosomes are extracellular vesicles released by cells that carry proteins, lipids and nucleic acids and function in intercellular communication. Previously, we determined that exosomes released from Mycobacterium tuberculosis (M.tb)-infected macrophages carry mycobacterial proteins and lipids.

Exosomes and other extracellular vesicles in host-pathogen interactions.

An effective immune response requires the engagement of host receptors by pathogen-derived molecules and the stimulation of an appropriate cellular response. Therefore, a crucial factor in our ability to control an infection is the accessibility of our immune cells to the foreign material. Exosomes-which are extracellular vesicles that function in intercellular communication-may play a key role in the dissemination of pathogen- as well as host-derived molecules during infection.

Exosomes isolated from mycobacteria-infected mice or cultured macrophages can recruit and activate immune cells in vitro and in vivo.

More than 2 billion people are infected with Mycobacterium. tuberculosis; however, only 5-10% of those infected will develop active disease. Recent data suggest that containment is controlled locally at the level of the granuloma and that granuloma architecture may differ even within a single infected individual.

Exosomes released from M. tuberculosis infected cells can suppress IFN-γ mediated activation of naïve macrophages.

Background: Macrophages infected with Mycobacterium tuberculosis (M.tb) are known to be refractory to IFN-γ stimulation. Previous studies have shown that M.

Mannose receptor-dependent delay in phagosome maturation by Mycobacterium avium glycopeptidolipids.

The ability of pathogenic mycobacteria to block phagosome-lysosome fusion is critical for its pathogenesis. The molecules expressed by mycobacteria that inhibit phagosome maturation and the mechanism of this inhibition have been extensively studied. Recent work has indicated that mannosylated lipoarabinomannan (ManLAM) isolated from Mycobacterium tuberculosis can function to delay phagosome-lysosome fusion and that this delay requires the interaction of ManLAM with the mannose receptor (MR).

A comparative study of host response to three Mycobacterium tuberculosis PE_PGRS proteins.

Three Mycobacterium tuberculosis proteins, PE_PGRS 16 (Rv0977), PE_PGRS 26 (Rv1441c) and PE_PGRS 33 (Rv1818c), were expressed in Mycobacterium smegmatis and used to investigate the host response to members of this unique protein family. Following infection of macrophages with the recombinant M. smegmatis (Ms) strains, Ms-PE_PGRS 33 and Ms-PE_PGRS 26 were significantly more persistent (4.