[Research progress on the Mycobacterium tuberculosis infection of mesenchymal stem cells]

Following Mycobacterium tuberculosis (Mtb) infection, the pathogen can establish a metabolically quiescent or replication-arrested dormant state within the host, leading to asymptomatic latent tuberculosis infection (LTBI). Under specific conditions, these dormant bacilli may reactivate and replicate, resulting in symptomatic clinical infection and constituting a major reservoir for active tuberculosis (TB). Dormant Mtb exhibits reduced susceptibility to conventional anti-TB drugs, and current TB vaccines fail to prevent the establishment or reactivation of dormant Mtb, rendering latent infection a major challenge in TB control. The formation of Mtb dormancy requires a unique microenvironment characterized by hypoxia, nutrient deprivation, and host immunosuppression. As an intracellular pathogen, Mtb primarily infects macrophages. Recent studies have revealed that Mtb can also infect mesenchymal stem cells (MSCs), where it persists in a dormant state for a long term. MSCs exhibit a microenvironment marked by hypoxia, cellular quiescence, lipid droplet biogenesis, and elevated autophagic activity. Moreover, MSCs exert immunosuppressive effects on the host immune response to Mtb, thereby facilitating the formation of bacterial dormancy and long-term intracellular survival, which further contributes to TB reactivation and relapse. This review summarizes current advances in understanding Mtb infection of MSCs and the underlying mechanisms associated with Mtb dormancy within this cellular niche.