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首页> 外文期刊>Clinical and experimental allergy : >Allergic sensitization is enhanced in early life through toll-like receptor 7 activation.
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Allergic sensitization is enhanced in early life through toll-like receptor 7 activation.

机译：通过Toll样受体7的活化，过敏性致敏作用在生命早期得到增强。

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BACKGROUND: Prospective cohort studies suggest that children hospitalized in early life with severe infections are significantly more likely to develop recurrent wheezing and asthma. OBJECTIVE: Using an inhalational mouse model of allergic airways inflammation, we sought to determine the effect of viral and bacterial-associated molecular patterns on the magnitude of the allergic inflammatory response and whether this effect was age dependent. METHODS: BALB/c mice were sensitized by intranasal administration of endotoxin(low) ovalbumin (OVA) in the absence or presence of viral single-stranded (ss)RNA, lipoteichoic acid or flagellin as neonates (within the first 24 h of life) or as weanlings (4 weeks of age). Mice were challenged four times with OVA at 6 weeks of age and end-points (bronchoalveolar lavage cytology, histology, antigen-specific T and B cell responses) determined at 7 weeks of age. RESULTS: Inhalational sensitization (<24 h or 4 weeks of age) and challenge with OVA induced a mild allergic inflammatory response in the airways as indicated by increased numbers of eosinophils and mucus cells, elevated serum OVA-specific IgG1, and production of T helper 2 (Th2) cytokines. Mice sensitized to endotoxin(low) OVA at birth in the presence of ssRNA or lipoteichoic acid, but not flagellin, showed an increase in the numbers of airway and tissue eosinophils, mucus producing cells and antigen-specific production of IL-13 as compared with mice exposed only to endotoxin(low) OVA. By contrast, all three TLR ligands failed to increase the magnitude of OVA-induced allergic inflammation in mice sensitized as weanlings. CONCLUSIONS: Recognition of distinct microbial-associated patterns in early life may preferentially promote the de novo differentiation of bystander, antigen-specific CD4(+) T cells toward a Th2 phenotype, and promote an asthma-like phenotype upon cognate antigen exposure in later life.
机译：背景：前瞻性队列研究表明，在生命早期住院并患有严重感染的儿童明显更有可能复发性喘息和哮喘。目的：使用吸入性小鼠过敏性气道炎症模型，我们试图确定病毒和细菌相关分子模式对过敏性炎症反应程度的影响，以及该影响是否与年龄有关。方法：在不存在或存在病毒单链（ss）RNA，脂磷壁酸或鞭毛蛋白作为新生婴儿的情况下（生命的头24小时内），通过鼻内给予低水平卵清蛋白（OVA）敏化BALB / c小鼠或断奶（4周龄）。在6周龄时用OVA攻击小鼠四次，并在7周龄时确定终点（支气管肺泡灌洗细胞学，组织学，抗原特异性T和B细胞反应）。结果：吸入致敏（<24小时或4周龄）和OVA刺激在气道中引起轻度过敏性炎症反应，表现为嗜酸性粒细胞和粘液细胞数量增加，血清OVA特异性IgG1升高以及T辅助物的产生2（Th2）细胞因子。与ssRNA或脂蛋白酸（而非鞭毛素）存在时对内毒素（低）OVA致敏的小鼠相比，气道和组织嗜酸性粒细胞，粘液产生细胞以及IL-13的抗原特异性产生数量增加。只暴露于内毒素（低）OVA的小鼠。相比之下，在断奶致敏的小鼠中，所有三种TLR配体均未能增加OVA诱导的过敏性炎症的程度。结论：在生命早期识别不同的微生物相关模式可能优先促进旁观者抗原特异性CD4（+）T细胞从头向Th2表型分化，并在以后的同源抗原暴露后促进哮喘样表型。 。

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