Abstract
BackgroundInflammatory bowel disease (IBD) is characterized by disturbance of pro-inflammatory cytokines and anti-inflammatory cytokines. Previous studies have demonstrated the effect of anti-inflammatory cytokines, such as interleukin-10 (IL-10) or IL-4 on IBD, but their data were controversial. This study further investigated the effect of IL-4 (IL-4), IL-10 and their combination on treatment of trinitrobenzenesulfonic acid (TNBS)-induced murine colitis.MethodspcDNA3.0 carrying murine IL-4 or IL-10 cDNA was encapsulated with LipofectAMINE 2000 and intraperitoneally injected into mice with TNBS-induced colitis. The levels of intestinal IL-4 and IL-10 mRNA were confirmed by quantitative-RT-PCR. Inflamed tissues were assessed by histology and expression of interferon (IFN)-γ, tumor necrosis factor (TNF)-α and IL-6.ResultsThe data confirmed that IL-4 or IL-10 over-expression was successfully induced in murine colon tissues after intraperitoneal injection. Injections of IL-4 or IL-10 significantly inhibited TNBS-induced colon tissue damage, disease activity index (DAI) and body weight loss compared to the control mice. Furthermore, expression of IFN-γ, TNF-α and IL-6 was markedly blocked by injections of IL-4 or IL-10 plasmid. However, there was less therapeutic effect in mice injected with the combination of IL-4 and IL-10.ConclusionsThese data suggest that intraperitoneal injection of IL-4 or IL-10 plasmid was a potential strategy in control of TNBS-induced murine colitis, but their combination had less effect.
Highlights
Inflammatory bowel disease (IBD) is characterized by disturbance of pro-inflammatory cytokines and anti-inflammatory cytokines
Gene transfection of trinitrobenzenesulfonic acid (TNBS)-treated mice To assess the effect of pcDNA3.0-IL-4 or pcDNA3.0-IL10 on TNBS-induced colitis, we intraperitoneally injected these plasmids into mice mixed with liposome 24 h after TNBS injection (Table 1) according to previous studies [23,24,25,26,27,28,29,30]
Effects of IL-4 and IL-10 on treatment of TNBS-induced microscopic injury of colon tissues In the TNBS-induced colitis model, we found that TNBS induced the colon tissues to severe inflammation, e.g. thickening of the colon wall and a high level of leukocyte infiltration (Figure 2A)
Summary
Inflammatory bowel disease (IBD) is characterized by disturbance of pro-inflammatory cytokines and anti-inflammatory cytokines. Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is characterized by chronic and relapsing inflammation of the gastrointestinal tract that leads to the destruction of the intestinal tissues. IBD affects approximately 1.4 million patients in the United States and 2.2 million people in Europe [1]. IL-4, as an anti-inflammatory cytokine, is less well elucidated in IBD It possesses immunoregulatory and immunosuppressive effects in the gut through mediating the differentiation of naive T cells to Th2 cell and inducing Th2-type CD4+ T cells to shift towards a Th1 response [16,17,18,19]. The efficacy of IL-4 treatment in murine IBD models is contentious [21]
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