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Lentinan ameliorates burn sepsis by attenuating CD4+ CD25+ Tregs.
- Source :
-
Burns (03054179) . Nov2016, Vol. 42 Issue 7, p1513-1521. 9p. - Publication Year :
- 2016
-
Abstract
- <bold>Aim: </bold>The aim of our study was to investigate the effect of lentinan on regulatory T cells (Tregs) in sepsis, especially on the generation of interleukin (IL)-10 via regulation of Erk-FoxO1 signaling.<bold>Methods: </bold>BalB/c mice were randomized into five groups: sham group, the group with burns plus Pseudomonas aeruginosa infection, and the groups with burns plus P. aeruginosa infection administered 40, 100, and 250mg/kg of lentinan. The mice were sacrificed on postburn days 0, 1, 2, 3, and 4, respectively, with eight animals per group at each time point. The peripheral blood CD4+ CD25+ Tregs and CD4+ T cells were isolated using magnetic microbeads. The phenotypes were analyzed by flow cytometry. The cytokine levels were determined with enzyme-linked immunosorbent assay (ELISA). Signal transduction was studied by Western blot, quantitative polymerase chain reaction (qPCR), and luciferase assay.<bold>Results: </bold>The IL-10-producing capacity of CD4+ CD25+ Tregs was significantly enhanced in the group with burns plus P. aeruginosa infection, compared with the sham group. Administration of lentinan significantly decreased IL-10 production and FoxP3 expression of CD4+ CD25+ Tregs. The proliferative activities of CD4+ T cells, however, were restored. Lentinan decreased lipopolysaccharide (LPS)-induced IL-10 production in the Tregs isolated from burned mice. In addition, lentinan attenuated LPS-stimulated Erk-FoxO1 activation.<bold>Conclusions: </bold>Lentinan may improve the outcome of postburn sepsis by suppressing LPS-triggered Erk-FoxO1 activation. Consequently, the hyperfunction of CD4+ CD25+ Tregs is inhibited, leading to a shift in the inflammatory status from Th2 to Th1 in postburn sepsis. [ABSTRACT FROM AUTHOR]
- Subjects :
- *SEPTICEMIA treatment
*POLYSACCHARIDES
*BURN patients
*CD4 antigen
*CD25 antigen
*T cells
*INTERLEUKIN-10
*FORKHEAD transcription factors
*THERAPEUTICS
*PHYSIOLOGY
*ANIMAL experimentation
*IMMUNOMODULATORS
*BURNS & scalds
*CELL physiology
*CELLULAR signal transduction
*ENZYME-linked immunosorbent assay
*FLOW cytometry
*GLUCANS
*INTERLEUKIN-2
*INTERLEUKINS
*MICE
*POLYMERASE chain reaction
*PSEUDOMONAS
*PSEUDOMONAS diseases
*SEPSIS
*WESTERN immunoblotting
*REVERSE transcriptase polymerase chain reaction
*PHARMACODYNAMICS
Subjects
Details
- Language :
- English
- ISSN :
- 03054179
- Volume :
- 42
- Issue :
- 7
- Database :
- Academic Search Index
- Journal :
- Burns (03054179)
- Publication Type :
- Academic Journal
- Accession number :
- 118542518
- Full Text :
- https://doi.org/10.1016/j.burns.2016.04.003