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Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Mannose prevents acute lung injury through mannose receptor pathway and contributes to regulate PPARγ and TGF-β1
Xuan-Li Xu1, Pei Zhang1, Yi-Hong Shen1
1Department of Respiratory Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine Hangzhou 310003, PR China.
Abstract:
Mannose has been reported to prevent acute lung injury (ALI), and mannose receptor (MR) has been demonstrated to have a role. The rationale for this study is to characterize the mechanism by which mannose and MR prevent lipopolysaccharide (LPS)-induced ALI. Male ICR mice were pretreated mannose by intravenous injection 5 min before and 3 h after intratracheal instillation of LPS. Pathological changes, proinflammatory mediator, peroxisome proliferator activated receptor gamma (PPARγ), MR, and transforming growth factor β1 (TGF-β1) levels were determined. The RAW264.7 cells were pretreated with mannose and stimulated with LPS for 3 h. Proinflammatory mediator and TGF-β1 in the culture media, PPARγ, MR, and TGF-β1 expression in RAW 264.7 cells were measured. Mannose markedly attenuated the LPS-induced histological alterations and inhibited the production of proinflammatory mediator in mice and in RAW 264.7 cells. Mannose increased PPARγ and MR expression, and inhibited TGF-β1 stimulated by LPS. Interestingly, competitive inhibition of MR with mannan was associated with elimination of the anti-inflammatory effects of mannose, and reversed effects of mannose of regulation to PPARγ and TGF-β1. MR is important in increasing PPARγ and decreasing TGF-β1 expression and plays a critical role in mannose's protection against ALI.
Insights
Mannose prevents acute lung injury (ALI) by activating the mannose receptor (MR). This mechanism involves increasing PPARγ and decreasing TGF-β1, crucial for mannose
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Acute lung injury (ALI) is a critical condition with significant morbidity.
- Mannose has shown potential in preventing ALI, with the mannose receptor (MR) implicated.
Purpose of the Study:
- To elucidate the mechanism by which mannose and MR protect against lipopolysaccharide (LPS)-induced ALI.
- To investigate the roles of PPARγ and TGF-β1 in this protective pathway.
Main Methods:
- Male ICR mice were treated with mannose before and after LPS instillation.
- RAW264.7 cells were treated with mannose and stimulated with LPS.
- Histological changes, inflammatory mediators, PPARγ, MR, and TGF-β1 levels were assessed.
Main Results:
- Mannose significantly reduced LPS-induced lung damage and inflammatory mediator production in vivo and in vitro.
- Mannose increased PPARγ and MR expression while inhibiting LPS-induced TGF-β1.
- Blocking MR with mannan abolished mannose's anti-inflammatory effects and reversed its regulatory impact on PPARγ and TGF-β1.
Conclusions:
- The mannose receptor (MR) plays a critical role in mannose-mediated protection against ALI.
- Mannose exerts its protective effects by upregulating PPARγ and downregulating TGF-β1 expression via MR activation.
