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The role of innate immunity in asthma: leads and lessons from mouse models.

机译：先天免疫在哮喘中的作用：小鼠模型的经验教训。

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According to the Hygiene Hypothesis, respiratory infections should protect individuals from allergic diseases including asthma, but epidemiologic data on the role of infections or exposure to microbial compounds in asthma are contradictory. Meanwhile, a number of murine models of airway sensitization are available facilitating the elucidation of pathways involved in asthma pathogenesis. Such studies have linked antigen presentation by activated pulmonary dendritic cells (DCs) with airway sensitization. Toll-like receptors (TLRs), which play a major role in innate immunity by sensing various microbial compounds, are expressed on DCs, as well as on mast cells (MCs). Activation of TLRs by administration of specific bacterial ligands, in particular lipopolysaccharide, can augment airway sensitization in mice, and there is evidence that this process involves TLR-dependent activation of DCs. Intriguingly, viral infection has been shown to increase airway inflammation in a murine asthma model via activation of DCs as well. TLR-4-dependent stimulation of MCs may also play a role in allergic sensitization in mice, and in vitro studies in murine cells show that ligation of TLRs expressed on MCs enhances degranulation. Therefore, evidence obtained from studies on mice indicates that innate immune responses may promote, rather than protect from, the development as well as the exacerbation of asthma.
机译：根据卫生假说，呼吸道感染应保护个人免受包括哮喘在内的过敏性疾病的侵害，但有关感染或接触微生物化合物在哮喘中的作用的流行病学数据却是矛盾的。同时，可利用多种鼠类气道致敏模型来促进哮喘发病机理的阐明。此类研究将激活的肺树突状细胞（DC）的抗原呈递与气道致敏联系起来。 DC以及肥大细胞（MC）上表达的Toll样受体（TLR）在先天免疫中起着主要作用，它们通过感知各种微生物化合物发挥作用。通过施用特定的细菌配体（特别是脂多糖）激活TLR，可以增强小鼠的气道致敏性，并且有证据表明，该过程涉及TLR依赖的DC激活。有趣的是，在鼠哮喘模型中，病毒感染也通过激活DC来增加气道炎症。 TLR-4依赖的MCs刺激也可能在小鼠的过敏性致敏中起作用，并且在鼠细胞中进行的体外研究表明，MCs上表达的TLRs的连接可增强脱粒作用。因此，从对小鼠的研究中获得的证据表明，先天性免疫应答可能促进而不是预防哮喘的发展和恶化。

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