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首页> 外文期刊>Clinical and experimental allergy : >Modification of allergic inflammation in murine model of rhinitis by different bacterial ligands: involvement of mast cells and dendritic cells.
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Modification of allergic inflammation in murine model of rhinitis by different bacterial ligands: involvement of mast cells and dendritic cells.

机译：通过不同的细菌配体修饰鼻炎小鼠模型中的过敏性炎症：肥大细胞和树突状细胞的参与。

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Background It has been suggested that airway bacterial infections exacerbate allergic disorders, and bacterial components in the air affect allergic inflammation via Toll-like receptors expressed on mast cells and dendritic cells in the airway mucosa. Objective Peptidoglycan (PGN) is a major component of the bacterial cell wall. We investigated the effect of PGN on the effector phase of allergic inflammation, in comparison with the effect of CpG-oligodeoxynucleotides (CpG), which is known to be a Th1 adjuvant. Methods Ovalbumin (OVA)-sensitized mice were challenged intranasally with OVA alone or OVA together with PGN or CpG. Nasal allergic symptoms and eosinophilia were scored, and the OVA-specific cytokine response was examined in the cells of cervical lymph nodes and nasal mucosa. Bone marrow-derived mast cells (BMMCs) and dendritic cells (BMDCs) were stimulated with PGN or CpG in vitro, and the expression level of cytokines and chemokines was examined by RT-PCR. In addition, the expression level of chemokines was examined by RT-PCR in mast cells of OVA-sensitized mice challenged with OVA alone or OVA together with PGN or CpG. Results PGN exposure exacerbated the nasal allergic symptoms and eosinophilia, whereas CpG exposure suppressed them. In addition, PGN exposure increased the OVA-specific IL-4 response in the cells, whereas CpG exposure decreased it. On the other hand, there were no significant differences in the OVA-specific IFN-gamma response. PGN but not CpG induced the expression of thymus and activation-regulated chemokine (TARC) and macrophage/monocyte-derived chemokine (MDC) in both BMMCs and mast cells of mice sensitized and challenged with OVA. CpG but not PGN induced the expression of IFN-beta and interferon-inducible protein-10 (IP-10) in BMDCs, and histamine did not influence this effect. Conclusion These results demonstrate that PGN exposure exacerbates allergic inflammation mainly via mast cells, whereas CpG exposure suppresses allergic inflammation mainly via dendritic cells.
机译：背景技术已经提出气道细菌感染加剧了过敏性疾病，并且空气中的细菌成分通过在气道粘膜中肥大细胞和树突状细胞上表达的Toll样受体影响过敏性炎症。客观肽聚糖（PGN）是细菌细胞壁的主要成分。与已知为Th1佐剂的CpG-寡脱氧核苷酸（CpG）的作用相比，我们研究了PGN对过敏性炎症效应期的作用。方法用卵清蛋白（OVA）致敏的小鼠单独用OVA或OVA连同PGN或CpG鼻内攻击。对鼻过敏症状和嗜酸性粒细胞进行评分，并在宫颈淋巴结和鼻粘膜细胞中检查OVA特异性细胞因子反应。体外用PGN或CpG刺激骨髓源肥大细胞（BMMC）和树突状细胞（BMDC），并通过RT-PCR检测细胞因子和趋化因子的表达水平。另外，通过RT-PCR检查趋化因子在单独用OVA或OVA与PGN或CpG一起攻击的OVA致敏小鼠的肥大细胞中的表达水平。结果PGN暴露加剧了鼻过敏症状和嗜酸性粒细胞增多，而CpG暴露抑制了它们。此外，PGN暴露会增加细胞中OVA特异性的IL-4反应，而CpG暴露会降低它。另一方面，OVA特异性IFN-γ反应无明显差异。 PGN而非CpG诱导了OVMC致敏和攻击小鼠的BMMC和肥大细胞中胸腺和激活调节趋化因子（TARC）以及巨噬细胞/单核细胞衍生的趋化因子（MDC）的表达。 CpG而不是PGN诱导BMDC中IFN-β和干扰素诱导蛋白10（IP-10）的表达，而组胺并不影响这种作用。结论这些结果表明PGN暴露主要通过肥大细胞加剧过敏性炎症，而CpG暴露主要通过树突状细胞抑制过敏性炎症。

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