Fig. 9: ATG7 deficiency leads to reduced mitophagy, increased mtROS production, and mildly activates cell death in macrophages during NTM infection in vitro.

a–d Atg7 cWT and Atg7 cKO BMDMs were infected with Mabc-R (MOI of 1 or 3, a), Mabc-S (MOI of 1 or 5, b), Mav (MOI of 1 or 3, c), or Mint (MOI of 1 or 3, d) for the indicated times. Intracellular survival of NTM was determined by CFU assay. e Atg7 cWT and Atg7 cKO BMDMs were infected with Mabc-R (MOI of 3) for the indicated times. IL-6 levels were measured by ELISA. f Atg7 cWT and Atg7 cKO BMDMs were pretreated with lung homogenate supernatants (lung sup) for 4 h, followed by infection with Mabc-S (MOI of 1) for the indicated times. IL-6 levels were measured by ELISA. g Human primary MDMs were infected with Mabc-R (MOI of 3) for 1 day and then transduced with lentivirus expressing shNS or shATG7 for 36 h. Transduction efficiency was evaluated by qRT-PCR. h Human primary MDMs were transduced with lentivirus expressing shNS or shATG7, followed by infection with Mabc-R (MOI of 3; left) or Mabc-S (MOI of 3; right). Bacterial burden was assessed by CFU assay at 1 or 2 dpi, respectively. i, j Human primary MDMs were transduced with lentivirus expressing shNS or shATG7 and then infected with Mabc-R (MOI of 5, i) or Mav (MOI of 5, j) for 12 h or 24 h, respectively. The concentrations of IL-1β and TNF were measured using ELISA. Statistical significance was determined by two-sided one-way ANOVA (a–d, f, j) or two-tailed Student’s t tests (e, g, h). Data shown (means ± SEM) represent the combined results of triplicates from three independent experiments. dpi days post infection, NS non-specific, sup supernatant. Source data are provided as a Source Data file.