Remote intestinal changes following blast-induced thoracic trauma with transient hemorrhagic shock and hind-limb ischemia.

BACKGROUND: The intestine is both a driver and a target of posttraumatic organ dysfunction. However, it remains unclear whether, and to what extent an extra-abdominal trauma, such as thoracic trauma with transient hemorrhagic shock and hind-limb ischemia (THS), provokes remote intestinal alterations. METHODS: A post hoc analysis was performed using jejunal tissue from a standardized murine THS model. Histological, immunohistochemical, and molecular analyses evaluated epithelial integrity, barrier components, and immune responses 24 h after the insult. RESULTS: Histological assessment of the intestine revealed no overt morphological damage. Nonetheless, jejunal expression of Tnk1 and Ripk3 was significantly increased, indicating epithelial stress and activation of necroptotic signaling. Tight junction marker Tjp1 was upregulated, while Muc2 was reduced. Intestinal expression levels of Il6 and Ifng declined, paralleled by a decrease in CD3⁺ T cells, whereas Lcn2 levels increased. CONCLUSIONS: Thoracic trauma combined with transient hemorrhagic shock including hind-limb ischemia induces remote intestinal alterations, characterized by epithelial stress, compensatory barrier reinforcement, and reduced mucosal immunity. These findings highlight the gut's sensitivity to extra-abdominal trauma and its potential contribution to systemic injury propagation.