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Published on: May 21, 2018
The Mechanisms Involved in Mesenchymal Stem Cell Alleviation of Sepsis-Induced Acute Lung Injury in Mice: A Pilot
Background:
Acute lung injury is a common complication of sepsis in intensive care unit patients. Inflammation is among the main mechanisms of sepsis. Therefore, suppression of inflammation is an important mechanism for sepsis treatment. Mesenchymal stem cells (MSCs) have been reported to exhibit antimicrobial properties.
Objective:
The present study investigated the effects of MSCs on sepsis-induced acute lung injury.
Methods:
Male C57BL/6 mice underwent a cecal ligation and puncture (CLP) operation to induce sepsis and then received either normal saline or MSCs (1 × 106 cells intravenously) at 3 hours after surgery. Survival after surgery was assessed. Lung injury was assessed by histology score, the presence of lung edema, vascular permeability, inflammatory cell infiltration, and cytokine levels in bronchoalveolar lavage fluid. Finally, we tested nuclear factor kappa-light-chain-enhancer of activated B cells activation in lung tissue.
Results:
As expected, CLP caused lung injury as indicated by significant increases in the histopathology score, lung wet to dry weight ratio, and total protein concentration. However, mice treated with MSCs had amelioration of the lung histopathologic changes, lung wet to dry weight ratio, and total protein concentration. The levels of cytokines tumor necrosis factor alpha, interleukin 6, interleukin 1β, and interleukin 17 in bronchoalveolar lavage fluid were dramatically decreased after MSCs treatment. In contrast, expression of interleukin 10 was increased after MSCs treatment. Moreover, mice treated with MSCs had a higher survival rate than the CLP group. Neutrophil infiltration into bronchoalveolar lavage fluid was attenuated after MSCs injection, but the amounts of macrophages observed in the MSC group showed no significant differences compared with the CLP group. In addition, MSCs treatment significantly reduced nuclear factor kappa-light-chain-enhancer of activated B cells activation in lung tissue.
Conclusions:
Based on the above findings, treatment with MSCs dampened the inflammatory response and inhibited nuclear factor kappa-light-chain-enhancer of activated B cells activation in the mouse CLP model. Thus, MSCs may be a potential new agent for the treatment of sepsis-induced acute lung injury. (Curr Ther Res Clin Exp. 2020; 81:XXX-XXX).
Insights
Mesenchymal stem cells (MSCs) show promise in treating sepsis-induced acute lung injury by reducing inflammation and improving survival rates. This study demonstrates MSCs
Area of Science:
- Immunology
- Regenerative Medicine
- Critical Care Medicine
Background:
- Sepsis frequently leads to acute lung injury (ALI) in intensive care units.
- Inflammation is a key mechanism in sepsis pathogenesis, making its suppression a therapeutic target.
- Mesenchymal stem cells (MSCs) possess known antimicrobial and anti-inflammatory properties.
Purpose of the Study:
- To investigate the therapeutic effects of MSCs on sepsis-induced ALI.
- To evaluate MSCs' impact on lung injury markers and inflammatory responses in a sepsis model.
Main Methods:
- Sepsis was induced in mice via cecal ligation and puncture (CLP).
- Mice received either saline or MSCs intravenously 3 hours post-CLP.
- Lung injury was assessed through histology, edema, permeability, inflammatory cells, cytokines, and NF-κB activation.
Main Results:
- MSC treatment ameliorated lung injury, reducing histopathology scores and wet/dry weight ratios.
- MSC therapy significantly decreased pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-17) and increased anti-inflammatory IL-10.
- Survival rates were higher in the MSC-treated group, accompanied by reduced neutrophil infiltration and NF-κB activation.
Conclusions:
- MSCs effectively dampen the inflammatory response in a mouse model of sepsis-induced ALI.
- MSC treatment inhibits NF-κB activation, a critical inflammatory pathway.
- MSCs represent a potential therapeutic agent for managing sepsis-induced acute lung injury.
