Korean Red Ginseng Enhances Immunotherapeutic Effects of NK Cells via Eosinophils in Metastatic Liver Cancer Model

Metastasis decreases the survival rate of patients with liver cancer. Therefore, novel anti-metastatic strategies are needed. Korean Red Ginseng (KRG) is often ingested as a functional food with an immune-boosting effect. We investigated a combination of KRG and natural killer (NK) cells as a novel immunotherapy approach. SK-Hep1 cells were injected into the tail vein of NRGA mice to establish an experimental metastasis model. KRG, NK cells, or a combination of KRG and NK cells were administered. Tumor growth was observed using an in vivo imaging system, and metastatic lesions were evaluated by histological analysis and immunohistochemistry. Bioluminescence intensity was lower in the KRG and NK cell combination group than in the other groups, indicating that the combination treatment suppressed the progression of metastasis. CD56 expression was used as a NK cell marker and hematological analysis was performed. The combination treatment also decreased the expression of matrix metalloproteinases and the area of metastatic lesions in liver and bone tissues, as well as increased the eosinophil count. Expression of cytokines-related eosinophils and NK cells was determined by Western blotting analysis. The expression of interleukin 33 (IL33) was induced by the combination of KRG and NK cells. High IL33 expression was associated with prolonged overall survival in the Kaplan–Meier plotter. Our results suggest that KRG enhances the immune activity of NK cells by IL-33 through eosinophils and suppresses metastatic liver cancer progression.     

Crucial role of the interleukin 1 receptor family member T1/ST2 in T helper cell type 2-mediated lung mucosal immune responses.

T1/ST2 is an orphan receptor of unknown function that is expressed on the surface of murine T helper cell type 2 (Th2), but not Th1 effector cells. In vitro blockade of T1/ST2 signaling with an immunoglobulin (Ig) fusion protein suppresses both differentiation to and activation of Th2, but not Th1 effector populations. In a nascent Th2-dominated response, anti-T1/ST2 monoclonal antibody (mAb) inhibited eosinophil infiltration, interleukin 5 secretion, and IgE production. To determine if these effects were mediated by a direct effect on Th2 cells, we next used a murine adoptive transfer model of Th1- and Th2-mediated lung mucosal immune responses. Administration of either T1/ST2 mAb or T1/ST2-Ig abrogated Th2 cytokine production in vivo and the induction of an eosinophilic inflammatory response, but failed to modify Th1-mediated inflammation. Taken together, our data demonstrate an important role of T1/ST2 in Th2-mediated inflammatory responses and suggest that T1/ST2 may prove to be a novel target for the selective suppression of Th2 immune responses.     

丙酸倍氯米松纳米微囊对哮喘豚鼠体内嗜酸性粒细胞及黏附分子的影响

目的 探讨丙酸倍氯米松（BDP）聚乳酸-聚乙酸（PLGA）纳米缓释微囊对哮喘豚鼠体内嗜酸性粒细胞、细胞表面黏附分子及可溶性细胞间黏附分子-1（sICAM-1）的影响，阐明其抑制嗜酸性粒细胞浸润的可能机制。方法 采用荧光酶标记法、间接ELISA法测定哮喘豚鼠体内黏附分子及血、肺泡灌洗液（BALF）中嗜酸性粒细胞计数。结果 哮喘豚鼠血浆及BALF中嗜酸性粒细胞计数、sICAM-1的OD值显著高于正常组（P〈0．01），微囊组每3d给药1次治疗后明显下降（P〈0．05），同普通制剂组每日给药相比，差异无显著性。荧光显微镜下BLAF细胞沉淀悬液中，BDP微囊组、普通制剂治疗组可见带有荧光染色的细胞大小相对均匀、分布稀疏，模型组中可见大量染色细胞，大小不均、分布密集。结论 BDP纳米微囊制剂每3d给药1次能显著降低血浆、BALF中可溶性黏附分子及细胞表面黏附分子的含量，从而对炎性细胞募集至气道产生抑制作用。     

黄芪对儿童过敏性鼻炎哮喘综合征血清总免疫球蛋白E及嗜酸性粒细胞的影响

目的 观察黄芪对儿童过敏性鼻炎哮喘综合征血清总免疫球蛋白E（IgE）及嗜酸性粒细胞（EOS）计数水平的影响.方法 过敏性鼻炎哮喘综合征儿童30人,分别在服用黄芪前及服用黄芪1,3,6个月时,监测血清总lgE及EOS计数水平,观察血清总lgE及EOS计数水平的变化.结果 黄芪可使血清总lgE及EOS计数水平下降,在服用3,6个月时,血清总lgE及EOS计数水平下降明显,差异具有统计学意义.结论 黄芪能有效降低儿童过敏性鼻炎哮喘综合征血清总IgE及EOS计数水平,预防并控制过敏性鼻炎哮喘综合征.     

The analysis of eosinophil and lymphocyte phenotype following single dose of high‐dose methylprednisolone in two siblings with marked hypereosinophilia

The effect of single high‐dose methylprednisolone (HDMP) on eosinophil and lymphocyte phenotype in two siblings with marked hypereosinophilia was investigated. Since conventional dose steroids failed to produce a haematological and clinical response in case one, both children were given HDMP (20 mg/kg/day). Eosinophils and lymphocytes showed an activated state before treatment, characterized by marked expression of CD11b, CD18, CD45RO on eosinophils and increased HLA‐DR, CD95, CD18, CD38 on lymphocytes. Twenty‐four hours after administration of HDMP a dramatic reduction in peripheral blood eosinophil count was observed in both patients associated with phenotypic changes characterized by decreased expression of CD11b, CD18, CD13 and increased CD95 expression in one. Furthermore, HDMP treatment induced a drop in the expression of CD95 and CD18 on lymphocytes. These changes may suggest a suppressive role for HDMP on eosinophil and lymphocyte activation which may have contributed to the haematological and clinical response.     

Risk factors for eosinophilic esophagitis

Eosinophilic esophagitis (EoE) is a chronic antigen driven disease, whereby food and/or aeroallergens result in inflammation and luminal narrowing, and the clinical symptoms of dysphagia and food bolus obstruction events (FBOE). Established risk factors are male gender, Caucasian race and atopy. Increased risk amongst family members, and a single nucleotide polymorphism (SNP) in a gene coding thymic stromal lymphopoietin (TSLP) on the pseudoautosomal region of the X and Y chromosomes supports a genetic predisposition. Environmental factors including the timing and nature of food and aeroallergen exposure to the developing immune system may be important, whilst esophageal barrier function integrity and the influence of microbiota are worthy of future research.