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. 2021 Apr 19;13(8):11595–11609. doi: 10.18632/aging.202854

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Copyright: © 2021 Liu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Exo-MSCs-M.tb induced pro-inflammatory response through TLRs. (A) The protein levels of TLR2, TLR4, and MyD88 in the lung of TLR2^-/-, TLR4^-/-, and MyD88 ^-/- mice, respectively. (B) TNF-α levels in the lung of TLR2^-/- mice treated with Exo-MSCs-M.tb (20μg) (20μg), as detected by ELISA assay 24 hours after exosome treatment. (C) TNF-α levels in the lung of TLR4^-/- mice treated with Exo-MSCs-M.tb (20μg), as detected by ELISA assay 24 hours after exosome treatment. (D) TNF-α levels in the lung of MyD88 ^-/- mice treated with control (PBS), Exo-MSCs (20μg), and Exo-MSCs-M.tb (20μg), as detected by ELISA assay 24 hours after exosome treatment. (E) IL-12 p40 levels in the lung of C57BL/6 mice treated control (PBS), Exo-MSCs (20μg), and Exo-MSCs-M.tb (20μg). (F) TNF-α levels in the lung of C57BL/6 mice treated with control (PBS), Exo-MSCs (20μg), and Exo-MSCs-M.tb (20μg). (G) Neutrophil infiltration of C57BL/6 mice treated with control (PBS), Exo-MSCs (20μg), and Exo-MSCs-M.tb (20μg). *p < 0.05.