Hepatocellular Expression of Macrophage Migration Inhibitory Factor (MIF) Is Associated with Ischemia-Reperfusion Injury After Liver Transplantation.

INTRODUCTION

Ischemia-reperfusion injury (IRI) is a major determinant of initial graft function after liver transplantation (LT), directly influencing the incidence of early dysfunction and short-term clinical outcomes. Macrophage migration inhibitory factor (MIF), a pleiotropic cytokine involved in inflammatory pathways and mechanisms of cellular adaptation to oxidative stress, may play a modulatory role in IRI, although its immediate tissue behaviour in grafts remains poorly characterised.

METHODS

We retrospectively evaluated adult LT recipients who underwent post-reperfusion biopsies suitable for histological and immunohistochemical analysis. Immunohistochemical expression of MIF was quantified using the IHC Profiler plugin (ImageJ), whereas IRI was graded according to validated histopathological criteria.

RESULTS

Among 153 biopsies analysed, 103 met the eligibility criteria, with most cases showing absent or mild IRI (70.9%). Hepatocellular expression of MIF was predominantly weak or moderate. Stronger immunohistochemical staining for MIF was associated with lower IRI severity (p<0.05). MIF expression correlated with pre-transplant laboratory parameters, without association with steatosis or early outcomes, including retransplantation or death within 15 days.

CONCLUSION

The findings suggest that greater immunohistochemical expression of MIF at reperfusion is associated with lower IRI intensity, indicating a possible adaptive role for this cytokine during this critical phase. MIF emerges as a potential tissue marker complementary to traditional histopathological scoring, with relevance for graft assessment and use in contemporary liver perfusion strategies.