Senior author Dr. Lalita Ramakrishan, who studies how TB evades the body's immune system and manipulates the body's defenses for its own ends, noted that the study also suggests an explanation for the longstanding observation that tuberculosis infections begin in the comparatively sterile lower lungs.
In the upper respiratory tract, resident microbes and inhaled microbes of a variety of species signal their presence.
These tip-offs alert and attract many infection-fighting cells to the upper airways. The presence of other microbes in the upper airway may thereby help to keep TB infections at bay by creating a hostile environment.
To cause disease, TB bacteria must sneak through this well-patrolled area and head for parts of the lungs where fewer microbiocidal cells are policing.
Almost like intruders wearing a stocking over their faces to keep surveillance cameras from clearly recording their features, the TB pathogens produce particular types of fatty substances, or lipids, on their cell surfaces.
These lipids, abbreviated as PDIM, are already known to be associated with bacterial virulence. The researchers showed that PDIM lipids function by masking the underlying molecular patterns that would reveal their dangerous nature to macrophages, a first-line defense of infection-fighting cells.
At the same time, a related lipid - called PGL - on the bacterium's cell surface promotes the recruitment of cells described as permissive macrophages. These clean-up cells engulf but don't kill the TB pathogens. Instead, they take them across the lung lining, deep into the lung tissue where the bacteria can establish an infection.
The findings have been published online in the journal Nature.