Glutamine modulates CD8αα+ TCRαβ+ intestinal intraepithelial lymphocyte expression in mice with polymicrobial sepsis

Jai Nien Tung, Wan Yun Lee, Man Hui Pai, Wei Jao Chen, Chiu Li Yeh, Sung Ling Yeh

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Objectives: CD8αα+ T-cell receptor (TCR) αβ+ intestinal intraepithelial lymphocytes (IELs) were found to have a regulatory function in the mucosal immune system. Glutamine (GLN) is an amino acid with immunomodulatory effects. The aim of this study was to investigate the influences of GLN on the proportion of CD8αα+ TCRαβ+ IELs and associated inflammatory mediator gene expression in polymicrobial sepsis. Methods: Mice were randomly assigned to a normal (NC) group, a sepsis with saline (SS) group, or a sepsis with GLN (SG) group. The NC group was fed a chow diet. Sepsis was induced by cecal ligation and puncture (CLP). The SS group was administered saline, and the SG group was given 0.75 g GLN/kg body weight via a tail vein after CLP. Mice were sacrificed 12 h after CLP, and CD8αα+ TCRαβ+ IELs were isolated for further analysis. Results: Sepsis resulted in a lower percentage of CD8αα+ TCRαβ+ IELs, and higher messenger (m)RNA expression of complement 5a receptor, interleukin (IL)-2 receptor β, IL-15 receptor α, and interferon-γ by CD8αα+ TCRαβ+ IELs. These immunomodulatory mediator genes decreased, whereas IL-7 receptor and transforming growth factor-β expressions increased in CD8αα+ TCRαβ+ IELs in septic mice with GLN administration. Annexin V/7-AAD staining revealed significantly lower apoptotic rates of CD8αα+ TCRαβ+ IELs in the SG group. Conclusion: A single dose of GLN administered after the initiation of sepsis increased the percentage of CD8αα+ TCRαβ+ IELs, prevented apoptosis of CD8αα+ TCRαβ+ IELs, and downregulated CD8αα+ TCRαβ+ IEL-expressed inflammatory mediators. These results suggest that GLN influenced the distribution and cytokine secretion of the CD8αα+ TCRαβ+ IEL subset, which may ameliorate sepsis-induced inflammatory reactions and thus mitigate the severity of intestinal epithelial injury.

Original languageEnglish
Pages (from-to)911-917
Number of pages7
JournalNutrition
Volume29
Issue number6
DOIs
Publication statusPublished - Jun 2013

Fingerprint

T-Cell Antigen Receptor
Glutamine
Sepsis
Lymphocytes
Punctures
Ligation
Interleukin-15 Receptors
Interleukin-7 Receptors
Anaphylatoxin C5a Receptor
Interleukin-2 Receptors
Annexin A5
Lymphocyte Subsets
Transforming Growth Factors
Interferons
Tail
Veins
Immune System
Down-Regulation
Body Weight
Apoptosis

Keywords

  • Apoptosis
  • CD8αα TCRαβ IELs
  • Glutamine
  • Intraepithelial lymphocytes
  • Sepsis

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics

Cite this

Glutamine modulates CD8αα+ TCRαβ+ intestinal intraepithelial lymphocyte expression in mice with polymicrobial sepsis. / Tung, Jai Nien; Lee, Wan Yun; Pai, Man Hui; Chen, Wei Jao; Yeh, Chiu Li; Yeh, Sung Ling.

In: Nutrition, Vol. 29, No. 6, 06.2013, p. 911-917.

Research output: Contribution to journalArticle

Tung, Jai Nien ; Lee, Wan Yun ; Pai, Man Hui ; Chen, Wei Jao ; Yeh, Chiu Li ; Yeh, Sung Ling. / Glutamine modulates CD8αα+ TCRαβ+ intestinal intraepithelial lymphocyte expression in mice with polymicrobial sepsis. In: Nutrition. 2013 ; Vol. 29, No. 6. pp. 911-917.
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abstract = "Objectives: CD8αα+ T-cell receptor (TCR) αβ+ intestinal intraepithelial lymphocytes (IELs) were found to have a regulatory function in the mucosal immune system. Glutamine (GLN) is an amino acid with immunomodulatory effects. The aim of this study was to investigate the influences of GLN on the proportion of CD8αα+ TCRαβ+ IELs and associated inflammatory mediator gene expression in polymicrobial sepsis. Methods: Mice were randomly assigned to a normal (NC) group, a sepsis with saline (SS) group, or a sepsis with GLN (SG) group. The NC group was fed a chow diet. Sepsis was induced by cecal ligation and puncture (CLP). The SS group was administered saline, and the SG group was given 0.75 g GLN/kg body weight via a tail vein after CLP. Mice were sacrificed 12 h after CLP, and CD8αα+ TCRαβ+ IELs were isolated for further analysis. Results: Sepsis resulted in a lower percentage of CD8αα+ TCRαβ+ IELs, and higher messenger (m)RNA expression of complement 5a receptor, interleukin (IL)-2 receptor β, IL-15 receptor α, and interferon-γ by CD8αα+ TCRαβ+ IELs. These immunomodulatory mediator genes decreased, whereas IL-7 receptor and transforming growth factor-β expressions increased in CD8αα+ TCRαβ+ IELs in septic mice with GLN administration. Annexin V/7-AAD staining revealed significantly lower apoptotic rates of CD8αα+ TCRαβ+ IELs in the SG group. Conclusion: A single dose of GLN administered after the initiation of sepsis increased the percentage of CD8αα+ TCRαβ+ IELs, prevented apoptosis of CD8αα+ TCRαβ+ IELs, and downregulated CD8αα+ TCRαβ+ IEL-expressed inflammatory mediators. These results suggest that GLN influenced the distribution and cytokine secretion of the CD8αα+ TCRαβ+ IEL subset, which may ameliorate sepsis-induced inflammatory reactions and thus mitigate the severity of intestinal epithelial injury.",
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AU - Lee, Wan Yun

AU - Pai, Man Hui

AU - Chen, Wei Jao

AU - Yeh, Chiu Li

AU - Yeh, Sung Ling

PY - 2013/6

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N2 - Objectives: CD8αα+ T-cell receptor (TCR) αβ+ intestinal intraepithelial lymphocytes (IELs) were found to have a regulatory function in the mucosal immune system. Glutamine (GLN) is an amino acid with immunomodulatory effects. The aim of this study was to investigate the influences of GLN on the proportion of CD8αα+ TCRαβ+ IELs and associated inflammatory mediator gene expression in polymicrobial sepsis. Methods: Mice were randomly assigned to a normal (NC) group, a sepsis with saline (SS) group, or a sepsis with GLN (SG) group. The NC group was fed a chow diet. Sepsis was induced by cecal ligation and puncture (CLP). The SS group was administered saline, and the SG group was given 0.75 g GLN/kg body weight via a tail vein after CLP. Mice were sacrificed 12 h after CLP, and CD8αα+ TCRαβ+ IELs were isolated for further analysis. Results: Sepsis resulted in a lower percentage of CD8αα+ TCRαβ+ IELs, and higher messenger (m)RNA expression of complement 5a receptor, interleukin (IL)-2 receptor β, IL-15 receptor α, and interferon-γ by CD8αα+ TCRαβ+ IELs. These immunomodulatory mediator genes decreased, whereas IL-7 receptor and transforming growth factor-β expressions increased in CD8αα+ TCRαβ+ IELs in septic mice with GLN administration. Annexin V/7-AAD staining revealed significantly lower apoptotic rates of CD8αα+ TCRαβ+ IELs in the SG group. Conclusion: A single dose of GLN administered after the initiation of sepsis increased the percentage of CD8αα+ TCRαβ+ IELs, prevented apoptosis of CD8αα+ TCRαβ+ IELs, and downregulated CD8αα+ TCRαβ+ IEL-expressed inflammatory mediators. These results suggest that GLN influenced the distribution and cytokine secretion of the CD8αα+ TCRαβ+ IEL subset, which may ameliorate sepsis-induced inflammatory reactions and thus mitigate the severity of intestinal epithelial injury.

AB - Objectives: CD8αα+ T-cell receptor (TCR) αβ+ intestinal intraepithelial lymphocytes (IELs) were found to have a regulatory function in the mucosal immune system. Glutamine (GLN) is an amino acid with immunomodulatory effects. The aim of this study was to investigate the influences of GLN on the proportion of CD8αα+ TCRαβ+ IELs and associated inflammatory mediator gene expression in polymicrobial sepsis. Methods: Mice were randomly assigned to a normal (NC) group, a sepsis with saline (SS) group, or a sepsis with GLN (SG) group. The NC group was fed a chow diet. Sepsis was induced by cecal ligation and puncture (CLP). The SS group was administered saline, and the SG group was given 0.75 g GLN/kg body weight via a tail vein after CLP. Mice were sacrificed 12 h after CLP, and CD8αα+ TCRαβ+ IELs were isolated for further analysis. Results: Sepsis resulted in a lower percentage of CD8αα+ TCRαβ+ IELs, and higher messenger (m)RNA expression of complement 5a receptor, interleukin (IL)-2 receptor β, IL-15 receptor α, and interferon-γ by CD8αα+ TCRαβ+ IELs. These immunomodulatory mediator genes decreased, whereas IL-7 receptor and transforming growth factor-β expressions increased in CD8αα+ TCRαβ+ IELs in septic mice with GLN administration. Annexin V/7-AAD staining revealed significantly lower apoptotic rates of CD8αα+ TCRαβ+ IELs in the SG group. Conclusion: A single dose of GLN administered after the initiation of sepsis increased the percentage of CD8αα+ TCRαβ+ IELs, prevented apoptosis of CD8αα+ TCRαβ+ IELs, and downregulated CD8αα+ TCRαβ+ IEL-expressed inflammatory mediators. These results suggest that GLN influenced the distribution and cytokine secretion of the CD8αα+ TCRαβ+ IEL subset, which may ameliorate sepsis-induced inflammatory reactions and thus mitigate the severity of intestinal epithelial injury.

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