Mycobacterium abscessus resides within lipid droplets and acquires a dormancy-like phenotype in adipocytes.

Mycobacterium abscessus (M. abscessus) is an emerging, rapidly growing mycobacterium that causes chronic lung infection, particularly in patients with cystic fibrosis, as well as skin and soft tissue infections. Adipose tissue is recognized as an important niche that supports M. tuberculosis persistence. However, the dormancy, latency, and persistence mechanisms of M. abscessus in the host remain poorly understood. This study investigated how adipose tissue serves as a niche for M. abscessus using both a human adipose tissue ex vivo infection model and a murine adipose tissue in vivo infection model. M. abscessus infected not only the cytosol of adipocytes but also entered host lipid droplets, where it formed intracytoplasmic lipid inclusions in the bacterial cell. To our knowledge, this unique localization has never been reported for M. abscessus or any other mycobacterium. Within host lipid droplets, M. abscessus lost acid-fastness and gained Nile Red positivity. These results suggest that M. abscessus acquires a dormancy-like phenotype within host lipid droplets of adipocytes, potentially contributing to its persistence, virulence, and resistance to treatment. These findings provide valuable insights into mycobacterial persistence mechanisms and could offer a promising foundation for developing novel therapeutic approaches.