It has been extensively studied in several mouse models how chronic, in particular chronic psychosocial, stressors facilitate the (re)activity of the innate immune system and, consequently, drive stress-associated pathologies. Here we first summarize the resulting concept and underlying mechanisms, proposing that social stress-induced bone marrow myelopoiesis, priming, emigration and activation of newly formed myeloid cells and accumulation of these cells in the spleen, gut, brain and fracture hematoma promote septic shock, colitis, anxiety and disturbed fracture healing, respectively. We further propose and discuss the hypothesis that it is not the social character of a particular stressor that promotes splenic invasion and subsequent full activation of stress-induced myeloid cells, but rather the occurrence of bite wounds as a result of direct physical interaction. Finally, we discuss the hypothesis that it is the combination of chronic stress, regardless of whether social or non-social in nature, and any kind of planned (i.e. surgery) or unplanned (i.e. bite wounds, injury) physical trauma that drives splenic invasion and subsequent full activation of stress-induced myeloid cells.

中文翻译：

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身体创伤在社会压力诱导的免疫激活中的作用。

在几种小鼠模型中，已经广泛研究了慢性应激物，特别是慢性心理应激物如何促进先天免疫系统的（再）活性，从而驱动与压力相关的病理。在这里，我们首先总结一下由此产生的概念和潜在机制，并提出社会压力诱导的骨髓骨髓生成，新形成的髓样细胞的引发，迁移和激活以及这些细胞在脾脏，肠道，脑和骨折血肿中的积累会促进败血性休克，结肠炎，焦虑症和骨折愈合不良。我们进一步提出并讨论了以下假设，即不是特定的应激源的社会特性会促进脾脏侵袭并随后完全激活应激诱导的髓样细胞，而是直接物理相互作用导致咬伤的发生。最后，我们讨论一个假说，无论是社会性还是非社会性的，都是慢性压力与任何类型的计划性（即手术）或非计划性（即咬伤，伤害）驱动脾脏侵袭的组合并随后完全激活应激诱导的髓样细胞。