Multifaceted intestinal defense following experimental blunt abdominal trauma

Blunt abdominal trauma (AT) can cause significant intestinal injury and act as a trigger for remote posttraumatic organ dysfunction, including the development of multi-organ dysfunction syndrome (MODS). A deeper understanding of its impact on intestinal barrier integrity and immune regulation is essential for developing therapeutic strategies that support posttraumatic recovery. We assessed jejunal tissue 24 hours following a standardized murine blast-induced direct blunt AT. Histological, immunohistochemical, proteome profiling, Western Blot, and molecular analyses were applied to assess epithelial integrity, barrier-associated proteins, intestinal mucus composition, and immune responses. The jejunum showed no trauma-specific histomorphological changes. Consistently, the expression of key epithelial barrier proteins, such as E-cadherin and tight-junction protein 1, remained stable or were even upregulated. Local inflammatory responses were evident; AT induced activation of defense-related pathways, accompanied by a marked increase in S100A8 expression and enhanced infiltration of CD3+ T cells. Mucus-covered areas of the intestinal surface were reduced, although transcriptional levels of MUC2 and C1GALT1 were elevated. In addition, the antimicrobial peptide CRAMP was upregulated in jejunal tissue following injury. These findings suggest that the intestine initiates a multifaceted protective response to blunt AT, characterized by barrier preservation, mucus alterations, and adaptive immune activation. Remarkably, although the trauma was sufficient to elicit an inflammatory reaction, it simultaneously activated mechanisms that reinforced epithelial integrity and compensatory processes that may counteract barrier disruption in the early posttraumatic phase.