Something old, something new: indoor endotoxin, allergens and asthma.
Something old, something new: indoor endotoxin, allergens and asthma.
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DOI：
10.1016/s1526-0542(04)90013-9
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发表时间：
2004-01-01
影响因子：
5.8
通讯作者：
Liu, Andrew H
中科院分区：
文献类型：
--
作者：
Liu, Andrew H
内毒素和过敏原暴露在哮喘的背景下已经被探索了一个多世纪。在知识金字塔的基础上，最近的观察为这些暴露对哮喘发展的影响提供了新的见解。其中一些研究挑战了一些以前持有的关于这些暴露在哮喘发病中的作用的概念。室内过敏原被公认为致敏哮喘患者炎症的基础，有助于疾病的严重程度。那么，更多地暴露于室内过敏原是否也会导致过敏原敏化和哮喘？虽然对屋尘螨的敏感度通常会随着暴露水平的增加而增加，但这似乎并不适用于猫，因为猫的过敏原暴露水平越高，敏感度就越低。事实上，最近的几项研究表明，儿童早期接触动物，如室内宠物或耕作马厩，与哮喘、花粉热和吸入性过敏原敏感性的发病率较低相关。哮喘的内毒素也提供了类似的悖论。内毒素是所有革兰氏阴性菌细菌细胞壁的一种强大的免疫刺激成分。因此，内毒素在我们的环境中无处不在。暴露于内毒素已经被很好地证明是棉花工人“星期一哮喘”或水杨症的基础，自那以后，内毒素暴露已成为广泛的职业环境中哮喘样症状的常见原因。哮喘患者对吸入内毒素特别敏感，吸入会引起即刻和持续的气流阻塞。内毒素暴露的悖论是，在生命早期接触更高水平的内毒素可能会缓解过敏和持续性哮喘的发展。由于在有动物的家里和不太可能发生过敏和哮喘的农业家庭中，内毒素暴露明显更高，早期生命中的内毒素和其他微生物暴露可能通过促进Th1型免疫发展来阻止过敏原敏化和哮喘的发展。这些观察结果与过敏和哮喘的“卫生假说”相一致，是对早期免疫调节方法用于哮喘治疗和预防的可能性的令人鼓舞的一瞥。
Endotoxin and allergen exposure have been explored in the context of asthma for more than a century. Building upon a pyramid of knowledge are recent observations that provide new insights to the effect of these exposures on the development of asthma. Some of these studies challenge some previously held concepts of the role of these exposures in asthma inception. Indoor allergens are well established as the basis of inflammation in sensitised asthmatics, contributing to disease severity. Then does greater exposure to indoor allergens cause allergen sensitisation and asthma as well? While risk of sensitisation to house dust mites generally increases with higher levels of exposure, this does not seem to hold for cats, where higher levels of cat allergen exposure are associated with less sensitisation. Indeed, several recent studies suggest that early childhood exposure to animals, as indoor pets or in farming stables, are associated with a lower prevalence of asthma, hay fever, and inhalant allergen sensitisation. Endotoxin in asthma provides a similar paradox. Endotoxin is a potent immune-stimulatory component of the bacterial cell wall of all gram-negative bacteria. As such, endotoxin is ubiquitous in our environment. Endotoxin exposure has been well demonstrated to underlie "Monday Asthma" or byssinosis in cotton workers, and has since emerged as a frequent cause of asthma-like symptoms in a wide range of occupational settings. Asthmatics are particularly sensitive to inhaled endotoxin, and inhalation induces both immediate and sustained airflow obstruction. The paradox of endotoxin exposure is that higher levels of exposure in early life might mitigate the development of allergy and persistent asthma. With endotoxin exposure being significantly higher in homes with animals and in farming households, where allergy and asthma are less likely to develop, endotoxin and other microbial exposures in early life may keep allergen sensitisation and asthma from developing by promoting Th1-type immune development. These observations, consistent with the "Hygiene Hypothesis" of allergy and asthma, are an encouraging glimpse of the potential for early immune modulatory approaches to asthma therapy and prevention.