Overshooting inflammation during the early phase after blunt thorax trauma promotes the development of acute respiratory distress syndrome, multiple organ failure, and subsequent mortality. Given that individuals diagnosed with stress-related disorders are characterized by chronic low-grade inflammation, we hypothesize that “psychosocial traumatic preload” poses a risk factor for the abovementioned complications after thorax trauma.
Here, we used the chronic subordinate colony housing (CSC) paradigm to induce “psychosocial traumatic preload” and systemic low-grade immune activation in male mice, indicated by elevated plasma concentrations of different inflammatory mediators. Subsequent thorax trauma was induced in anaesthetized mice by a single blast wave centered on the thorax; SHAM animals were exposed to anesthesia only. Mice were killed 2, 6, and 24 h after thorax trauma or SHAM treatment.
Independent of thorax trauma, CSC caused an increase in adrenal weight, and a decrease in thymus weight, indicating that the stress paradigm worked reliably. Moreover, although lung histology was not affected by prior stress, CSC exposure aggravated the early immune response after thorax trauma, indicated by elevated myeloperoxidase lung concentrations in thorax trauma-exposed CSC versus respective single-housed control (SHC) mice (2 h). Furthermore, thorax trauma caused an increase in total bronchoalveolar lavage fluid (BAL) protein (24 h), BAL C5a (2 h), BAL cell counts (24 h), and BAL keratinocyte chemoattractant (6 h and 24 h) in CSC but not SHC mice.
Our data indicate that repeated psychosocial traumatization during adulthood moderately aggravates the local immune response toward thorax trauma, but overall may be considered as a rather minor risk factor in terms of thorax trauma-associated complications.