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. 2021 Jul 22;12:695278. doi: 10.3389/fimmu.2021.695278

Table 1.

The differences between macrophages and MSCs after Mtb infection.

Item Macrophages MSCs
LDs IFN-γ/HIF-1α promotes the formation of intracellular LDs (53); lower levels of LDs accumulation (26 Mechanism is unknown; high levels of LDs accumulation (26
IFN-γ stimulation Activating macrophages to kill Mtb; The expression of ROS increased; No increase in PGE2 release (54) The CFU of intracellular Mtb increased in a dose-dependent manner; ROS production is not affected; The expression of PGE2 increased; increasing autophagy flux (23)
Phagocytosis of Mtb Mannose receptor (MR) is a major receptor (55) MR was not involved (25)
Autophagy Decreasing Mtb viability (56)
Autophagy is induced by activated macrophages (56, 57)
Intracellular Mtb growth restriction; MSCs have inherent autophagy (25)
Intracellular Mtb Active replication (22); no significant change in morphology (26); most of Mtb are located to early endosomes immediately after infection (22) No proliferation and dormancy state (22, 25); increasing bacterial cell density and reduction in cell size (26); Most of Mtb are located in cytosol (22)
Cellular states Cells die at very low levels of infection (26) Cells enter into a quiescent state (22)
Oxidizing reaction Releasing lower levels of NO (58) Releasing higher levels of NO (25)
Phagocytic ability of Mtb Stronger (22) Weaker (22)
Mtb efflux pumps Rv0194, Rv1218c, Rv1272c, Rv1273c, Rv1463, Rv1687c, Rv2686c, Rv2687c, Rv2688c, Rv1348, Rv1349, Rv3239c, Rv3728, Rv1183, Rv1146, Rv0969, Rv3578 (59) ABC transporters ABCC1 and ABCG2 (23)
HHS Vulnerability Disclosure