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  4. Effects of the Glutamine Administration on T Helper Cell Regulation and Inflammatory Response in Obese Mice Complicated with Polymicrobial Sepsis
 
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Effects of the Glutamine Administration on T Helper Cell Regulation and Inflammatory Response in Obese Mice Complicated with Polymicrobial Sepsis

Journal
Mediators of inflammation
Journal Volume
2020
Date Issued
2020
Author(s)
Yeh, Chiu-Li
Su, Li-Han
JIN-MING WU  
PO-JEN YANG  
PO-CHU LEE  
PO-DA CHEN  
CHUN-CHIEH HUANG  
Hsieh, Der-Yirng
Wang, Hsueh-Ju
Yeh, Sung-Ling
MING-TSAN LIN  
DOI
10.1155/2020/8869017
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/535715
Abstract
This study investigated the impacts of GLN on inflammation and T cell dysregulation in obese mice complicated with sepsis. Mice were divided into normal control (NC) and high-fat diet groups. The high-fat diet provided 60% of energy from fat and was administered for 10 weeks to induce obesity. Mice fed with a high-fat diet were then assigned to sham (SH) and sepsis with saline (SS) or GLN (SG) groups. The SH group was subjected to laparotomy, while the sepsis group underwent cecal ligation and puncture (CLP). The SS group was intravenously injected with saline. The SG group was intravenously administered GLN after CLP. Mice were sacrificed at 12, 24, or 48 h post-CLP, respectively. Results demonstrated that in the presence of obesity, sepsis drove CD4+ T cells toward the helper T (Th)2 and Th17 lineages. Also, expressions of inflammatory cytokines and macrophage infiltration markers in adipose tissues and lungs were elevated. Treatment of obese mice with GLN after sepsis reversed Th polarization and downregulated macrophage infiltration and inflammatory cytokine, whereas the tight junction-associated protein expression increased in the lungs. These findings suggest that the intravenous administration of GLN to obese mice after sepsis modulated a more balanced Th cell lineage, alleviated inflammation, and attenuated lung injury.
SDGs

[SDGs]SDG2

[SDGs]SDG3

Other Subjects
adiponectin; bupivacaine; CD68 antigen; epidermal growth factor; glutamine; glyceraldehyde 3 phosphate dehydrogenase; interleukin 1beta; interleukin 6; leptin; occludin; protein bcl xl; protein ZO1; tiletamine plus zolazepam; transcription factor FOXP3; tumor necrosis factor; xylazine; adipocytokine; cytokine; glutamine; adipose tissue; animal cell; animal experiment; animal model; Article; CD4+ T lymphocyte; cecal ligation and puncture-induced sepsis; controlled study; down regulation; gene expression; helper cell; ileocecal valve; inflammation; lipid diet; macrophage; male; mouse; nonhuman; obesity; postoperative pain; protein expression; regulatory T lymphocyte; T lymphocyte subpopulation; Th17 cell; Th2 cell; tight junction; animal; blood; body weight; C57BL mouse; CD4+ T lymphocyte; cytology; drug effect; helper cell; immunology; inflammation; laparotomy; lung injury; metabolism; microbiology; mouse mutant; sepsis; Adipokines; Adipose Tissue; Animals; Body Weight; CD4-Positive T-Lymphocytes; Cytokines; Glutamine; Inflammation; Laparotomy; Lung Injury; Macrophages; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Sepsis; T-Lymphocytes, Helper-Inducer; Tight Junctions
Type
journal article

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