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.
According to the researchers on this study, these mechanisms appear to allow certain TB pathogens to avoid detection by the pattern recognition receptors that enable some infection-fighting cells to spot a variety of different disease microbes through the pathogen-associated molecular patterns on or near their cell surface.
Like most other bacteria, TB pathogens have many of these telltale molecular patterns that should activate an immune response. However, TB pathogens have evolved mechanisms to circumvent tripping the alarm, in this case by physically masking the otherwise detectable pattern. This cover-up allows them to infect the airway initially by avoiding the infection-fighting cell populations that are detrimental to their survival, the researchers noted.
The TB pathogens then use the other lipid molecule, PGL, to co-opt a host chemical pathway that triggers the recruitment of the permissive macrophages.
The present study expands on earlier work in the Ramakrishan and collaborative labs, which helped describe the strategies by which TB pathogens manipulate host pathways for their own purposes after they enter certain host cells.
These include the secretion of proteins that help expand the niche for TB by recruiting macrophages to the early lung tubercles characteristic of the disease. The present study describes earlier stages in infection, when the pathogens first come in contact with their potential h
|Contact: Leila Gray|
University of Washington