Rhodococcus equi is a bacterium which can cause lung disease in young foals which is very similar to tuberculosis in humans. Rhodococcus equi is closely related to the tubercle bacillus Mycobacterium tuberculosis.
In the Bonn Institute of Cell Biology Eugenia Fernandez and Marco Polidori in Professor Albert Haas’s team have been examining why Rhodococcus equi is not killed and digested in macrophages, and is even able to multiply there. In the course of this study the group was able to demonstrate that the rhodococci are able to put prevent the phagosome development inside the macrophage, preventing acidification and merging with the lysosomes. As a result the bacteria are not exposed to the large array of lysosomal digestive enzymes and acid.
“What this means is that the rhodococci manipulate their host cell, they make it themselves comfortable in an environment free of acid and digestive enzymes and multiply there,” Haas comments. Within a few days after the onset of the infection, the macrophages die of the infection, they disintegrate and release the multiplied pathogens.
The Bonn cell biologists have demonstrated in the past that this cell death is ‘necrotic’. This means that cell components escape, attract other immune cells and activating them. Ultimately the result is inflammation and tissue damage. “It is quite possible that rhodococci do not really mind this,” Professor Haas says, “since they can then grab a passing macrophage and colonise fresh material.”
The next aim of the Bonn researchers is to investigate which bacterial features are important for preventing the merger of phagosomes and lysosomes, and how the immune system normally successfully eradicates an infection despite all the tricks the bacteria use.
MEDICA.de; Source: Institute of Cell Biology of the University of Bonn