Abstract
This study investigated the effects of dietary glutamine (Gln) on T-helper (Th) and T regulatory (Treg) cell homeostasis and colonic inflammatory mediator expression in mice with dextran sulfate sodium (DSS)-induced colitis. Mice were randomly assigned to 4 groups with 2 normal control (C and G) and 2 DSS-treated groups (DC and DG). The C and DC groups were fed a common semipurified diet, while the G and DG groups received an identical diet except that part of the casein was replaced by Gln, which provided 25% of the total amino acid nitrogen. Mice were fed the diets for 10 days. On day 6, mice in the normal control groups were given distilled water, while those in the DSS groups were given distilled water containing 1.5% DSS for 5 d. At the end of the experiment, the mice were sacrificed for further examination. Results showed that DC group had higher plasma haptoglobin, colonic weight, immunoglobulin G, inflammatory cytokine and nuclear factor (NF)-κB protein levels. Gln administration lowered inflammatory mediators and NF-κB/IκBα ratio in colitis. Compared with the DC group, the percentages of interleukin-17F and interferon-γ in blood and transcription factors, T-bet and RAR-related orphan receptor-γt, gene expressions in mesenteric lymph nodes were lower, whereas blood Foxp3 was higher in the DG group. Also, DG group had lower colon injury score. These results suggest that Gln administration suppressed Th1/Th17 and Th-associated cytokine expressions and upregulated the expression of Tregs, which may modulate the balance of Th/Treg and reduce inflammatory reactions in DSS-induced colitis.
Highlights
Inflammatory bowel disease (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), refers to chronic inflammatory disorders that may affect the entire gastrointestinal tract [1]
Our results showed that compared with the mixed amino acid solution group, Gln administration reduced inflammatory mediator production and leukocyte infiltration into tissues [21]
We analyzed the distribution of blood T cell populations including Th1, Th2, Th17, Th22, and T regulatory (Treg) cells, because the balance between Th and Treg cells and the cytokine profiles derived from these T cells play major roles in the inflammation of IBD [12,25,26]
Summary
Inflammatory bowel disease (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), refers to chronic inflammatory disorders that may affect the entire gastrointestinal tract [1]. CD4+ helper T (Th) cells play major roles in both the induction and persistence of IBD by producing proinflammatory cytokines. A recent study suggested that the Th17-cell-driven immune response, which produces excess IL-17A, IL-17F, and IL-22, plays a critical role in the pathogenesis of both CD and UC [7]. The intestinal mucosa is normally maintained in an equilibrium state in which the protective immunity and tolerance to self-antigens and commensal bacteria are balanced. This tolerance is maintained by Treg cells in the gut by inhibiting the proliferation and effector functions of other T cells [11]. Recent studies indicated that IBD is associated with a decrease in Treg cells and increase in Th17 cells in peripheral blood [12,13]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
