Study of immunomodulatory effects of mesenchymal stem cell-derived exosomes in a mouse model of LPS induced systemic inflammation

Eshghi, Fateme; Tahmasebi, Safa; Alimohammadi, Mona; Soudi, Sara; Khaligh, Sahar Ghaffari; Khosrojerdi, Arezou; Heidari, Neda; Hashemi, Seyed Mahmoud

doi:10.1016/j.lfs.2022.120938

Cited by 26 publications

(8 citation statements)

References 61 publications

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“…Similarly, a significant GRAN is produced, leading to an exacerbated inflammatory response [ 52 ]. Moreover, RBC, PLT, and LYM decrease after the organism is stimulated by LPS, which results in inflammation [ 53 , 54 ].…”

Section: Resultsmentioning

confidence: 99%

Anti-Inflammatory Activity of Peptides from Ruditapes philippinarum in Lipopolysaccharide-Induced RAW264.7 Cells and Mice

Lin,

Shen,

Jiang

et al. 2024

Foods

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In our previous study, two peptides with favorable anti-inflammatory effects, Asp-Gln-Thr-Phe (DQTF) and Gly-Tyr-Thr-Arg (GYTR), were screened from Ruditapes philippinarum using an in vitro–in silico strategy. The present study aims to investigate the ameliorative effect of Ruditapes philippinarum peptides (RPPs) on acute inflammation and clarify the potential mechanism through in vitro and in vivo experiments. The anti-inflammatory effects of DQTF and GYTR were verified with a lipopolysaccharide (LPS)-induced RAW264.7 cell acute inflammation model and the anti-inflammatory effect of the enzymatic hydrolysates of Ruditapes philippinarum was explored in vivo using an LPS-induced acute inflammatory injury model in mice. The results show that DQTF and GYTR improved the morphology of LPS-injured cells and decreased the concentrations of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in LPS-induced cells. Moreover, the antioxidant enzyme activity in cells was markedly increased with DQTF and GYTR. The enzymatic hydrolysates of Ruditapes philippinarum were obtained with hydrolysis using pepsin–chymotrypsin–trypsin (PeCTHC) and pepsin–trypsin (PeTHC), respectively. PeCTHC and PeTHC significantly reduced pro-inflammatory cytokines and nitric oxide (NO) in the serum. Additionally, the blood indices and levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and malondialdehyde (MDA) in the livers of mice were markedly improved with RPPs administration. In conclusion, RPPs have preventive and protective effects on acute inflammation, with significant prospects for development in the field of functional foods.

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Section: Resultsmentioning

confidence: 99%

Anti-Inflammatory Activity of Peptides from Ruditapes philippinarum in Lipopolysaccharide-Induced RAW264.7 Cells and Mice

Lin,

Shen,

Jiang

et al. 2024

Foods

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“…Hazrati et al reported that the combination of MSC-derived exosomes and imipenem can effectively reduce the secretion of NO, TNF-α, and IL-1β inflammatory mediators in the E. coli -infected HepG2 cells ( 16 ). Eshghi et al also reported that MSC-derived exosomes can decrease the levels of IL-1β and TNF-α inflammatory cytokines and ameliorate the subsequent destructive effects of inflammation caused by sepsis in a mouse model of LPS-induced systemic inflammation ( 33 ). Khosrojerdi et al also reported that the mesenchymal stem cell-derived exosomes combined with imipenem can ameliorate inflammatory responses and liver damage in a sepsis mouse model ( 34 ).…”

Section: Discussionmentioning

confidence: 99%

Secretome of adipose derived-mesenchymal stem cells reduces the Vibrio cholerae attachment to Caco-2 cells and subsequent inflammatory responses

Moulazade,

Soudi,

Bakhshi

2024

IJM

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Background and Objectives: Mesenchymal Stem Cells (MSCs) can repair gastrointestinal tract damage. The Secretome of MSCs has a high capacity to inhibit bacterial colonization and the subsequent inflammatory responses of Vibrio cholerae. Materials and Methods: The Caco-2 cells were treated with adipose-derived MSCs (AD-MSCs) secretome and then in- fected with V. cholerae. Subsequently, the bacterial attachment and invasion, cholera toxin gene expression, PGE2 and IL-6 secretion, TNF-α, IL-1β, and IL-8 expression, and apoptosis of Caco-2 cells were evaluated. Results: The secretome of AD-MSCs significantly reduced the V. cholerae attachment and internalization on Caco-2 epithe- lial cells (P<0.0001). The cholera toxin (Ctx-B) gene expression (FR=4.56 ± 0.66) and PGE2 production (P=0.0007) were also significantly reduced. The production of NO and TNF-α, IL-1β, and IL-8 pro-inflammatory cytokines were significantly (P<0.05) reduced in exposure to the secretome of AD-MSCs. Secretome also improved a significant 81.33% increase in IL-6 production (128.1 ± 37.6 pg/mL) and showed a 12.36% significant decrease in epithelial cell apoptosis (P< 0.0001) after exposure to V. cholerae. Conclusion: The secretome of AD-MSCs can play a critical role in inhibiting bacterial colonization, and subsequent inflam- matory responses, and maintaining the integrity of the epithelial barrier. The secretome may be effective in the prevention of hypovolemic shock.

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“…Inflammatory factors induce podocyte injury and promote DN progression through nuclear factor kappa B, toll-like receptors, and adenosine 5’-monophosphate-activated protein kinase signaling pathways [ 36 ]. Stem cell-derived exosomes have the potential to ameliorate the destructive effects of inflammatory factors and alleviate tissue damage, suggesting that the effect of ADSCs-Exo on podocyte injury and DN progression may be closely related to its anti-inflammatory and antioxidant functions [ 37 ]. We have previously found that HO-1 can inhibit podocyte apoptosis by up-regulating autophagy level [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Adipose-derived stem cell exosomes regulate Nrf2/Keap1 in diabetic nephropathy by targeting FAM129B

Ren

Qian

et al. 2023

Diabetol Metab Syndr

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Background Exosomes from adipose-derived stem cells (ADSCs-Exos) have exhibited a therapeutic role in diabetic nephropathy (DN). Further studies are needed to investigate how ADSCs-Exos regulate oxidative stress and inflammation in high glucose-induced podocyte injury. Methods An enzyme-linked immunosorbent assay (ELISA) was used to detect cellular inflammation. Reactive oxygen species (ROS) levels were assessed using flow cytometry in podocytes with different treatments. A malondialdehyde (MDA) kit was used to evaluate the lipid peroxidation levels in podocytes and kidney tissues of mice. Western blotting and co-immunoprecipitation were performed to detect protein expression and protein-protein interactions. Results ADSCs-Exos reversed oxidative stress and inflammation in podocytes and kidney tissues of DN mice induced by high glucose levels in vitro and in vivo. Interference with heme oxygenase-1 expression could reverse the improvement effect of ADSCs-Exos on oxidative stress induced by high glucose levels. Furthermore, high glucose inhibited nuclear factor erythroid 2-related factor 2 (Nrf2) protein expression and promoted Kelch-like ECH-associated protein 1 (Keap1) protein expression in podocytes, as well as their binding ability. As a potential target for Nrf2/Keap1 pathway regulation, FAM129B expression in podocytes is regulated by high glucose and ADSCs-Exos. Moreover, FAM129B siRNA blocked the inhibitory effect of ADSCs-Exos on intracellular ROS and MDA upregulation induced by high glucose in podocytes. Conclusion ADSCs-Exos regulate the Nrf2/Keap1 pathway to alleviate inflammation and oxidative stress in DN by targeting FAM129B, which may provide a potential therapeutic strategy for DN.

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Study of immunomodulatory effects of mesenchymal stem cell-derived exosomes in a mouse model of LPS induced systemic inflammation

Cited by 26 publications

References 61 publications

Anti-Inflammatory Activity of Peptides from Ruditapes philippinarum in Lipopolysaccharide-Induced RAW264.7 Cells and Mice

Anti-Inflammatory Activity of Peptides from Ruditapes philippinarum in Lipopolysaccharide-Induced RAW264.7 Cells and Mice

Secretome of adipose derived-mesenchymal stem cells reduces the Vibrio cholerae attachment to Caco-2 cells and subsequent inflammatory responses

Adipose-derived stem cell exosomes regulate Nrf2/Keap1 in diabetic nephropathy by targeting FAM129B

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