Abstract
ABSTRACT In this study, we examined whether Lactobacillus plantarum C29 could restore 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced T helper 17 (Th17)/regulatory T cells (Tregs) imbalance in mice. Treatment with C29 inhibited the differentiation of splenic T cells into Th17 cells and the expression of retinoic acid receptor-related orphan receptor gamma t (RORγt) and IL-17 in vitro, whereas promoting the differentiation into Tregs. Oral administration of Lactobacillus plantarum C29 in mice attenuated TNBS-induced colon shortening, myeloperoxidase (MPO) activity, inducible Nitric oxide (NO) synthase, and cyclooxygenase-2 expression, and activation of NF-κB in the colon of mice. C29 treatment downregulated TNF-α, IL-17, and IL-1β expression, while increasing IL-10 expression. C29 treatment suppressed TNBS-induced Th17 cell differentiation and reduced IL-17 and RORγt expression, while promoting the TNBS-suppressed Tregs differentiation and IL-10 and forkhead box P3 expression. These findings suggest that C29 can alleviate colitis by modulating NF-κB activation as well as Th17/Treg balance.
Highlights
Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn’s disease, is a chronically relapsing inflammatory disease of the gastrointestinal (GI) tract (Maloy & Powrie, 2011)
To investigate whether C29 could modulate the T cell differentiation involved in the adaptive immunity, we purified Th cells from mouse splenocytes, stimulated them with Th17differentiating cytokines in the presence or absence of C29, and measured subsets of T helper 17 (Th17) cells as well as the expression of the Th17-specific transcription factor RORγt and cytokine IL-17 using a flow cytometer and Quantitative real time – polymerase chain reaction (qPCR) (Figure 1)
The inflammatory cytokines TNF-α, IL-1β, IL-6, IL-10, and IL-23 are secreted by the innate immune system and regulate the proliferation and differentiation of T cells of the adaptive immune system into Th1, Th2, Th17, and Tregs (Geremia, Biancheri, Allan, Corazza, & Di Sabatino, 2014; Lord, 2015)
Summary
Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn’s disease, is a chronically relapsing inflammatory disease of the gastrointestinal (GI) tract (Maloy & Powrie, 2011). The stimulation of pathogens in the GI tracts is continuously defended by the gut immune system, which consists of neutrophils, macrophages, dendritic cells (DCs), and T cells involved in innate and adaptive immunity (Du et al, 2015; Niess et al, 2008; Nourshargh & Alon, 2014). Activation of innate immune cells, including DCs and macrophages, by these antigens stimulates the adaptive immune cells such as T cells: the secretion of TNF-α, IL-10, and IL-12 in the immune cells stimulate the differentiation of naïve CD4+ T cells into effector T cells, such as Th1, Th17, and regulatory T cells (Tregs) (Atreya, Atreya, & Neurath, 2008; Owen & Mohamadzadeh, 2013; Rutella & Locatelli, 2011).
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