FIGURE 1.

Environmental Mycobacterium abscessus (MABS) isolates have the smooth colony morphotype and express glycopeptidolipid (GPL). GPL in the outermost aspect of the cell wall “masks” underlying glycosylated lipoproteins such as phosphatidyl-myo-inositol mannosides (PIMs) involved in immune recognition and blocks the bacterial cell–cell interaction of lipids such trehalose polyphleates which may play a role in clumping and cord formation. By preventing MABS from being recognized by innate immune surveillance mechanisms and promoting biofilm formation, GPL facilitates colonization of bronchiectatic lung airways. After colonization, spontaneous or temperature sensitive loss of GPL is associated with “unmasking” of these molecules. This leads to recognition by TLR2 on macrophages and respiratory epithelial cells resulting in release of the proinflammatory cytokines TNFα (from macrophages) and IL-8 (from respiratory epithelial cells). Rough variants acquire a virulent phenotype characterized by the ability to grow in serpentine cords and cause macrophage apoptosis leading to rapid cell–cell spread and propagation of infection. Isolation of MABS rough variants from the sputum is associated with progressive lung infection.