Psychological Stress, Immunity, and the Effects on Indigenous Microflora
Psychological Stress, Immunity, and the Effects on Indigenous Microflora
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DOI：
10.1007/978-3-319-20215-0_11
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发表时间：
2016-01-01
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影响因子：
--
通讯作者：
Bailey, Michael T.
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文献类型：
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作者：
Bailey, Michael T.
心理压力是生活中固有的一部分，通过直接神经系统神经支配和神经内分泌激素的释放影响身体的所有器官。心理神经免疫学（PNI）领域已经清楚地证明，对心理压力源的生理反应可以极大地影响免疫系统的功能，从而确定了在压力时期加剧疾病易感性或严重性的一种方式。本章介绍了 PNI 和微生物内分泌学领域之间的交叉研究，以证明自然屏障防御（例如由共生微生物群提供的防御）可能会因暴露于心理压力源而被破坏。这些应激效应在妊娠应激条件下出生的动物以及微生物群发育成熟的老年动物的肠道微生物群的发育中很明显。此外，数据表明，暴露于不同类型的应激源会导致微生物群从皮肤和粘膜表面易位到区域淋巴结。综合考虑，就会出现这样一种情况：心理压力源诱发神经内分泌反应，有可能直接或间接影响共生微生物群、屏障防御的完整性和微生物的内化。最后，提出了一个假设，即在没有明显感染的情况下，应激源诱导的微生物群落变化有助于观察到的应激源诱导的炎症标志物的增加。
Psychological stress is an intrinsic part of life that affects all organs of the body through direct nervous system innervation and the release of neuroendocrine hormones. The field of PsychoNeuroImmunology (PNI) has clearly demonstrated that the physiological response to psychological stressors can dramatically impact the functioning of the immune system, thus identifying one way in which susceptibility to or severity of diseases are exacerbated during stressful periods. This chapter describes research at the interface between the fields of PNI and Microbial Endocrinology to demonstrate that natural barrier defenses, such as those provided by the commensal microflora, can be disrupted by exposure to psychological stressors. These stress effects are evident in the development of the intestinal microflora in animals born from stressful pregnancy conditions, and in older animals with fully developed microbial populations. Moreover, data are presented demonstrating that exposure to different types of stressors results in the translocation of microflora from cutaneous and mucosal surfaces into regional lymph nodes. When considered together, a scenario emerges in which psychological stressors induce a neuroendocrine response that has the potential to directly or indirectly affect commensal microflora populations, the integrity of barrier defenses, and the internalization of microbes. Finally, a hypothesis is put forth in which stressor-induced alterations of the microflora contribute to the observed stressor-induced increases in inflammatory markers in the absence of overt infection.