2017 Microbial pathogenesis

Polysaccharides from Citrus grandis L. Osbeck suppress inflammation and relieve chronic pharyngitis.

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Microbial pathogenesis Vol. 113 : 365-371 • Dec 2017

Chronic pharyngitis, a common inflammation of the pharyngeal mucosa, is often caused by bacteria, viruses, alcohol abuse, overuse of the voice and cigarettes. This study aimed to explore the effects of polysaccharides of Citrus grandis L. Osbeck (PCG) in relieving chronic pharyngitis and illustrate the underlying mechanisms. Polysaccharides were obtained from PCG by column chromatographic extraction. Six clinical symptom scores, such as the severity of itchy throat, hoarseness, pain, odynophagia, cough and otalgia were evaluated in chronic pharyngitis patients after the oral intake of PCG. The effects of polysaccharides on chronic pharyngitis were investigated in ammonia-stimulated rabbits through pathology analysis. The levels of inflammatory markers in the peripheral blood T cells were analyzed by ELISA. The total and phosphorylated levels of ERK1/2, JNK and p38 were assessed by Western blot. Protein amount of IKKalpha and p65, IKKalpha/beta activity and p65 activity were evaluated by Western blot and luciferase assay. The clinical studies presented that PCG significantly relieved the six symptoms of chronic pharyngitis patients. Pathology analysis of chronic pharyngitis animals showed that the PCG treatment groups showed a significant decrease in the number of pathologic cells and the reduction of pathologic cells was dose-dependent (p < 0.01). ELISA analysis showed that PCG significantly inhibited the alphaCD3-induced increase of IFN-gamma, IL-2 and IL-4 expression in a dose-dependent manner. Moreover, Western blot and luciferase assay suggested that the phosphorylation of IKKalpha/beta in peripheral blood T cells was inhibited by the administration of PCG. These results indicate that polysaccharides exhibit anti-inflammatory effects by inhibiting the phosphorylation of IKKs, subsequently suppressing the NF-kappaB pathway activation and decreasing the expression of inflammatory mediators.

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