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Hepatocytes express the antimicrobial peptide HBD-2 after multiple trauma: an experimental study in human and mice
Stefanie Fitschen-Oestern1, Matthias Weuster1, Sebastian Lippross1
1Department of Trauma Surgery, University Medical Center of Schleswig-Holstein, Campus Kiel, Arnold-Heller-Strasse 3, 24105, Kiel, Germany.
Background:
Human-beta defensins (HBD) belong to the family of acute phase peptides and hold a broad antimicrobial spectrum that includes gram-positive and gram-negative bacteria. HBD are up-regulated after severe injuries but the source of posttraumatic HBD expression has not been focused on before. In the current study we analysed the role of liver tissue in expression of HBD after multiple trauma in human and mice.
Methods:
HBD-2 expression has been detected in plasma samples of 32 multiple trauma patients (ISS > 16) over 14 days after trauma by ELISA. To investigate major sources of HBD-2, its expression and regulation in plasma samples, polymorphonuclear neutrophils (PMN) and human tissue samples of liver and skin were analysed by ELISA. As liver samples of trauma patients are hard to obtain we tried to review findings in an established trauma model. Plasma samples and liver samples of 56 male C57BL/6 N-mice with a thorax trauma and a femur fracture were analysed by ELISA, real-time PCR and immunohistochemistry for murine beta defensin 4 (MBD-4) and compared with the expression of control group without trauma. The induction of HBD-2 expression in cultured hepatocytes (Hep G2) was analysed after incubation with IL-6, supernatant of Staphylococcus aureus (SA) and Lipopolysaccharides (LPS). One possible signalling pathway was tested by blocking toll-like receptor 2 (TLR2) in hepatocytes.
Results:
Compared to healthy control group, plasma of multiple traumatized patients and mice showed significantly higher defensin levels after trauma. Compared to skin cells, which are known for high beta defensin expression, liver tissue showed less HBD-2 expression, but higher HBD-2 expression compared to PMN. Immunhistochemical staining demonstrated upregulated MBD-4 in hepatocytes of traumatised mice. In HepG2 cells HBD-2 expression could be increased by stimulation with IL-6 and SA. Neutralization of HepG2 cells with αTLR2 showed reduced HBD-2 expression after stimulation with SA.
Conclusion:
Plasma samples of multiple traumatized patients showed high expression of HBD-2, which may protect the severely injured patient from overwhelming bacterial infection. Our data support the hypothesis that liver is one possible source for HBD-2 in plasma while posttraumatic inflammatory response.
Insights
Liver tissue contributes to human beta-defensin (HBD) expression after severe trauma, potentially aiding in fighting bacterial infections. This study investigated HBD-2 in trauma patients and MBD-4 in mice, highlighting the liver
Area of Science:
- Immunology
- Trauma Research
- Antimicrobial Peptides
Background:
- Human beta-defensins (HBDs) are antimicrobial peptides with a broad spectrum, crucial in the acute phase response.
- HBDs are upregulated following severe injuries, but their precise sources post-trauma remain underexplored.
- This study investigates the role of liver tissue in HBD expression after multiple trauma in humans and mice.
Purpose of the Study:
- To determine if liver tissue is a significant source of human beta-defensin-2 (HBD-2) in plasma after multiple trauma.
- To analyze the expression and regulation of HBD-2 in human plasma, neutrophils, and liver tissue.
- To investigate murine beta-defensin-4 (MBD-4) expression in a mouse model of multiple trauma.
Main Methods:
- HBD-2 levels in plasma from 32 multiple trauma patients were measured using ELISA over 14 days.
- HBD-2 expression in human plasma, polymorphonuclear neutrophils (PMN), liver, and skin samples was analyzed.
- Murine beta defensin 4 (MBD-4) was quantified in plasma and liver samples from 56 mice with induced trauma using ELISA, real-time PCR, and immunohistochemistry.
Main Results:
- Plasma HBD-2 levels were significantly elevated in trauma patients and mice compared to controls.
- Liver tissue exhibited higher HBD-2 expression than PMN, though less than skin.
- Hepatocytes showed increased MBD-4 expression in traumatized mice; HBD-2 expression in cultured hepatocytes (HepG2) was induced by IL-6 and Staphylococcus aureus (SA), and partially mediated by TLR2.
Conclusions:
- Elevated HBD-2 in trauma patient plasma may offer protection against bacterial infections.
- The liver is identified as a potential source of post-traumatic HBD-2 in plasma.
- These findings contribute to understanding the innate immune response following severe injury.
