Table 1.

List of diverse cell types used for investigation of host-pathogen interactions between Mycobacterium tuberculosis (and model systems thereof) and different cell types at the mitochondrial interface.

	Cell type/model	Mycobacterial strain/ Mtb protein	MOI	Incubation post-infection	Impact on mitochondrial structure	Immunological consequence	Impact on non-mitochondrial bioenergetics	Impact on mitochondrial bioenergetics	Impact on cell fate	References
Human	THP-1	Mtb H37Rv	10 5	24 h 24 h	Increased electron density, with a clear and vivid definition of the cristae	Modest increase in TNF-α	Increased as compared to uninfected cells	Mitochondrial membrane transition potential was significantly increased than H37Ra Increase in this ATP/ADP ratio augments activity of the mitochondrial electron transport chain Decreased ATP (mitochondrial respiration) Oxygen consumption rate as in basal respiration, total respiration, proton leak, and TCA are all reduced as compared to uninfected THP-1	Modest increase in both apoptosis and necrosis	(Riendeau and Kornfeld, 2003; Jamwal et al., 2013; Asalla et al., 2017; Cumming et al., 2018)
		Dead Mtb	5	24 h			Slightly reduced as compared to untreated cells	Oxygen consumption rate as in basal respiration, total respiration, proton leak, and TCA are reduced slightly as compared to uninfected THP-1 but much higher than Mtb or BCG	No effect	(Cumming et al., 2018)
		Mtb H37Ra	10	24 h	A significant reduction in the electron density of the matrix outlines of the cristae were distinct and there was no gross pathology of the mitochondria	TNF-α		Mitochondrial membrane potential was significantly lower than H37Rv Decrease in this ATP/ADP ratio as compared to uninfected cells Decreased mitochondrial electron transport chain	Apoptosis	(Jamwal et al., 2013)
		BCG	10 5 1	24 h 2-72 h		Significant increase in TNF-α Significant release of CCL2 Activates macrophages	Non-mitochondrial respiration is more than that induced by Mtb	Generates superoxide radicals Oxygen consumption rate as in basal respiration, total respiration, proton leak, and TCA are all reduced as compared to uninfected THP-1but higher than Mtb	Significant increase in apoptosis	(Riendeau and Kornfeld, 2003; Méndez-Samperio et al., 2010; Chávez-Galán et al., 2016; Asalla et al., 2017; Cumming et al., 2018)
	U937	Mtb H37Rv Mtb H37Ra	10 10	1–5 days 1–5 days				ΔMMP increased greater with H37Rv than H37Ra but similarly with MOI > 5	Modest increase in apoptosis and necrosis (day3 onwards) Significant increase in apoptosis and not necrosis (day3 onwards)	(Danelishvili et al., 2003)
	Jurkat T cells	rRv1818c-Tat	1–15 μg/ml	24 h	Rv1818c localizes to mitochondria				Caspase dependent apoptosis	(Balaji et al., 2007)
	RD (sarcoma)	Transient expression of PE_PGRS33	1 μg plasmid with Lipofectamine	24 h	PE_PGRS33 localizes to mitochondria				Apoptosis (24 h onwards) and necrosis (late stage-48 h onwards)	(Cadieux et al., 2011)
	PBMC derived macrophages	Mtb H37Rv Mtb H37Ra LpqH	2–10 2–10 0.5–50 μg/ml	0–48 h 0–48 h 24 h				At MOI = 5, H37Rv caused more MMP and cytC release at 6 h At MOI-10, both H37Rv and H37Ra caused an equal release of cytC and back at 48 h	Modest increase in apoptosis 48 h and necrosis(72 h) Significant increase in apoptosis and modest increase in necrosis Caspase dependent apoptosis	(Chen et al., 2006; Sánchez et al., 2012)
	PBMC derived dendritic cells	Mtb H37Rv Mtb H37Ra Dead Mtb	1–10 1–10 1–10	24–48 h 24–48 h 24–48 h		DC maturation Il-1, Il-6, TNF-α. DC maturation Il-1, Il-6, TNF- α No DC maturation IL-6, IL-8, TNF- α secreted		Non-apoptotic cell death Non-apoptotic cell death No cell death	Caspase independent	(Ryan et al., 2011)
	alveolar epithelial cells (A549 type II epithelial cells)	Mtb Erdman Mtb CDC1551 M. bovis-BCG Mtb Erdman, an ESAT-6 deletion mutant M. smegmatis	10, 100 10 10, 100 50	6–24 h 48 h 6–48 h 6–24 h 48 h	No effect Fragmented, appear as spherical structures Decrease in mitochondrial mass (pronounced effect with MOI = 100) No effect on mitochondrial structure and mass No effect	No inflammasome activation		No effect No effect Significant decrease in MMP	Necrosis (post 48 h) Necrosis Necrosis (post 5 days) No cytotoxicity up to MOI = 50	(Dobos et al., 2000; Fine-Coulson et al., 2015)
Murine	macrophage cell line RAW 264.7	H37Rv rRv3261 rHBHA BCG	10–20 10 μg/ml 10	1–4 days 24 h 24 h	Localizes to mitochondria	Dose dependent LDH release ROS production TNF, IL-6, MCP-1 TNF-α and IL-6 are secreted		Loss of membrane potential, Bax translocation, Cyt C release Decrease in MMP, bax translocation, Cyt C release Decrease in MMP	Necrosis in a dose and time-dependent manner Caspase-3/9 dependent apoptosis Caspase dependent apoptosis Caspase dependent apoptosis	(Sohn et al., 2011; Wu et al., 2014; Jee et al., 2017; Lee et al., 2020)

The above list includes a diverse array of cell types used in mycobacterial research with details of variables of experimental conditions (Specific strain, MOI, incubation time post-infection) with mitochondria-associated readouts such as morphological changes, Bioenergetic changes, and cell fate. It is be noted that it is not an exhaustive list of all model cell types and mycobacterial strains used in mycobacterial research.