The role of physical trauma in social stress-induced immune activation

• Published in: Neuroscience and biobehavioral reviews Vol. 113; pp. 169 - 178
• Main Authors: Foertsch, Sandra, Reber, Stefan O.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Ltd 01-06-2020
• Subjects: Bacterial translocation; Bite wounds; CD11b+myeloid cells; Chronic psychosocial stress; Chronic subordinate colony housing (CSC); Functional glucocorticoid insensitivity; Inflammation; Myelopoiesis; Physical trauma; Social disruption stress (SDR); Bite wounds; Chronic psychosocial stress; Social disruption stress (SDR); Chronic subordinate colony housing (CSC); Inflammation; Physical trauma; Myelopoiesis; Functional glucocorticoid insensitivity; Bacterial translocation; CD11b+myeloid cells; CD11b(+)myeloid cells
• ISSN: 0149-7634; 1873-7528
• DOI: 10.1016/j.neubiorev.2020.02.025

•Social stress-induced myelopoiesis, priming and egress of myeloid cells critically depends on β-AR and IL-1R1 signaling.•Stress-induced accumulation of myeloid cells in the spleen requires physical trauma.•Full activation of myeloid cells from the bone marrow depends on bacterial translocation.•Functional in vitro GC resistance of myeloid splenocytes following social stress requires TLR4 activation.
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.