Leprosy-causing bacteria alter the behavior of the body’s macrophages, leading these normally protective immune cells to initiate nerve damage during early infection, a new NIAID-supported study in a zebrafish model shows. An international team of scientists found that a molecule on the bacteria’s surface, called phenolic glycolipid (PGL), is responsible for reprogramming the macrophages.
PGL is present on the surfaces of many pathogenic mycobacteria, including those that cause leprosy (Mycobacterium leprae) and tuberculosis(Mycobacterium tuberculosis). In a related NIAID-funded study using a zebrafish model of tuberculosis, the researchers found that mycobacterial PGL also helps the bacteria establish infection by escaping macrophage defenses. A small difference in the chemical structure of M. leprae PGL confers upon it the additional ability to contribute to nerve damage.
Findings from this pair of studies shed light on how nerve damage is initiated in leprosy and suggest PGL as a potential target for the development of strategies to prevent tuberculosis and other mycobacterial diseases. The studies appeared Aug. 24 in Cell and Immunity.