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Mycobacterium avium subsp.hominissuis is an opportunistic human pathogen that has been shown to form biofilmin vitro andin vivo . Biofilm formationin vivo appears to be associated with infections in the respiratory tract of the host. The reasoning behind howM. avium subsp.hominissuis biofilm is allowed to establish and persist without being cleared by the innate immune system is currently unknown. To identify the mechanism responsible for this, we developed anin vitro model using THP-1 human mononuclear phagocytes cocultured with establishedM. avium subsp.hominissuis biofilm and surveyed various aspects of the interaction, including phagocyte stimulation and response, bacterial killing, and apoptosis.M. avium subsp.hominissuis biofilm triggered robust tumor necrosis factor alpha (TNF-α) release from THP-1 cells as well as superoxide and nitric oxide production. Surprisingly, the hyperstimulated phagocytes did not effectively eliminate the cells of the biofilm, even when prestimulated with gamma interferon (IFN-γ) or TNF-α or cocultured with natural killer cells (which have been shown to induce anti-M. avium subsp.hominissuis activity when added to THP-1 cells infected with planktonicM. avium subsp.hominissuis ). Time-lapse microscopy and the TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) assay determined that contact with theM. avium subsp.hominissuis biofilm led to early, widespread onset of apoptosis, which is not seen until much later in planktonicM. avium subsp.hominissuis infection. Blocking TNF-α or TNF-R1 during interaction with the biofilm significantly reduced THP-1 apoptosis but did not lead to elimination ofM. avium subsp.hominissuis . Our data collectively indicate thatM. avium subsp.hominissuis biofilm induces TNF-α-driven hyperstimulation and apoptosis of surveilling phagocytes, which prevents clearance of the biofilm by cells of the innate immune system and allows the biofilm-associated infection to persist.

Mycobacterium avium Biofilm Attenuates Mononuclear Phagocyte Function by Triggering Hyperstimulation and Apoptosis during Early Infection