Journal
AGING-US
Volume 13, Issue 8, Pages 11595-11609Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/aging.202854
Keywords
mesenchymal stem cell; exosome; mycobacterium tuberculosis; pro-inflammatory response; toll-like receptor
Categories
Ask authors/readers for more resources
This study demonstrated that M.tb infection promoted the generation of Exo-MSCs-M.tb, which induced a pro-inflammatory response in macrophages by enhancing the production of inflammatory factors. The effect exhibited a time-dependent pattern with the peak inflammatory response observed at 72 hours post-infection of MSCs.
Tuberculosis (TB) is a common infectious disease caused by Mycobacterium tuberculosis (M.tb), and macrophages serve as the primary natural host of M.tb. Mesenchymal stem cells (MSCs)-derived exosomes play an essential role in inflammatory responses. This study aimed to determine the role of exosomes derived from M.tb-infected MSCs (Exo-MSCs-M.tb) on macrophages in vitro and in vivo and the underlying mechanisms. Here, we demonstrated that M.tb infection promoted the production of Exo-MSCs-M.tb, but did not influence MSCs proliferation. Exo-MSCs-M.tb were taken up by macrophages and then induced the pro-inflammatory response of macrophages through elevating the production of TNF-alpha, RANTES, and iNOS. Also, proinflammatory response induced by Exo-MSCs-M.tb displayed a time-dependent pattern in macrophages, in which the highest level of inflammatory response was observed at 72 hours post-infection of MSCs. In addition, the effect of Exo-MSCs-M.tb was mediated through TLR2/4 and MyD88 signaling pathways. Furthermore, ExoMSCs-M.tb could induce the pro-inflammatory response in mice in vivo, and exosomes isolated from Exo-MSCsM.tb-treated mice could also promote the pro-inflammatory response. Taken together, these results indicate that Exo-MSCs-M.tb induced the pro-inflammatory response of macrophages through TLRs signaling. This study provides new insight into the potential of MSCs-derived exosomes for the treatment of TB.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available