Saliva-mediated killing of intracellular bacteria

Identifier:  TFG:111

Handle: https://hdl.handle.net/20.500.11797/TFG111

Authors:  García García, Juncal

Abstract:
Saliva-mediated killing of intracellular bacteria Summary Mycobacterium tuberculosis is able to infect and survive in macrophages and this is pivotal for development of tuberculosis. Clearing of infection is difficult, which consequently leads to persistent infection. However, a novel process recently in macrophages has been discovered where macrophages form macrophages Extracellular Traps (METs), which is a mechanism similar to apoptosis that possible, could help to eliminate the pathogen. This process has also been observed in neutrophils (NETs), activated by a sialic-acid containing salivary component, mucins (data non-published). This process involves a process called autophagy, which results in the breakdown of structural proteins of the nuclear and plasma membrane that in turn facilitates the release of DNA. Previous studies also indicate that intracellular Mycobacterium tuberculosis is subject to elimination through autophagy of the infected cell. Surprisingly, we observed a similar effect wherein, peripheral blood monocytes demonstrated increased killing of intracellular mycobacteria after exposure to saliva. In this work, through different experiments, which we have been optimizing continuously, we exposed mycobacteria-infected monocytes (cell lines and peripheral blood monocytes) to saliva and examined the intracellular survival rate of the mycobacteria. Our result indicated that saliva stimulation mediated killing of intracellular mycobacteria but that free sialic acid did not show any apparent effect. Nevertheless, there are indications that the active component in saliva encompasses a sialic acid containing moiety. Though the results were not conclusive, promising preliminary results make it feasible to further explore the possibility that saliva could contain component(s) stimulating monocytes to kill mycobacteria and other intracellular pathogens.