Mannose prevents acute lung injury through mannose receptor pathway and contributes to regulate PPARγ and TGF-β1 level.
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.
Department of Respiratory Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine Hangzhou 310003, PR China.
Xuan-Li
XL
Xu
Department of Respiratory Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine Hangzhou 310003, PR China.
Pei
P
Zhang
Department of Respiratory Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine Hangzhou 310003, PR China.
Yi-Hong
YH
Shen
Department of Respiratory Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine Hangzhou 310003, PR China.
He-Quan
HQ
Li
Department of Respiratory Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine Hangzhou 310003, PR China.
Yue-Hong
YH
Wang
Department of Respiratory Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine Hangzhou 310003, PR China.
Guo-Hua
GH
Lu
Department of Respiratory Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine Hangzhou 310003, PR China.
Jian-Ying
JY
Zhou
D055371:Acute Lung Injury / Q000378:metabolism* / Q000517:prevention & control; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D015153:Blotting, Western; D002478:Cells, Cultured; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D037181:Lectins, C-Type / Q000378:metabolism*; D008297:Male; D008358:Mannose / Q000494:pharmacology*; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins / Q000378:metabolism*; D051379:Mice; D008813:Mice, Inbred ICR; D047495:PPAR gamma / Q000378:metabolism*; D060888:Real-Time Polymerase Chain Reaction; D011956:Receptors, Cell Surface / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D053773:Transforming Growth Factor beta1 / Q000378:metabolism*
D000893:Anti-Inflammatory Agents; D037181:Lectins, C-Type; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; D047495:PPAR gamma; D011956:Receptors, Cell Surface; D053773:Transforming Growth Factor beta1; D008358:Mannose
Acute lung injury; PPARγ; TGF-β1; anti-inflammation; mannose; mannose receptor