Mycobacterium abscessus induces CD18-dependent reactive oxygen species production in human mast cells

Mycobacterium abscessus (Mab) is an opportunistic pathogen that causes severe infections, especially in immunocompromised individuals. The role of human mast cells (hMCs) during Mab infection remains poorly characterized.
This study examines early interactions between Mab and hMCs, evaluating MC viability, degranulation, reactive oxygen species (ROS) production, cytokine secretion, and receptor expression following Mab exposure. MCs interacted with both smooth (ATCC 19977) and rough (clinical isolate) Mab morphotypes. Infection did not induce MC degranulation. Instead, Mab primarily stimulated intracellular ROS generation, Granzyme B, and IL-1β production. CD18 and CD46 were necessary for hMC-Mab interactions, and CD18 deficiency significantly impacted ROS production. hMC cytokine priming with IL-33 or IFN-_γ did not significantly affect CD18 expression, nor impact ROS production upon Mab infection. These findings demonstrate that MCs mount a rapid, receptor-dependent
intracellular response to Mab, highlighting an early and previously underappreciated role for MCs in Mab infection.