Heparin-Binding Protein and Transplant-Associated Inflammation: Emerging Roles in Infection, Ischemia–Reperfusion Injury, and Allograft Dysfunction

Heparin-binding protein (HBP) is an activation-dependent neutrophil granule protein involved in innate immune activation, endothelial barrier disruption, and inflammatory tissue injury. Although HBP has been extensively investigated in infectious diseases, particularly sepsis, its potential relevance to transplantation has only recently attracted attention. Several post-transplant complications, including infection, ischemia–reperfusion injury (IRI), microvascular dysfunction, and allograft rejection, share common pathological features such as neutrophil activation, endothelial injury, and excessive inflammatory amplification, suggesting a possible mechanistic role for HBP. This review summarizes the current understanding of HBP biology and evaluates its potential contribution to transplant-associated complications. We also discuss the feasibility of using HBP as an early biomarker for infection surveillance, inflammatory risk stratification, and graft injury monitoring. Furthermore, emerging therapeutic approaches targeting HBP or HBP-mediated vascular inflammation, including neutralizing antibodies, heparin derivatives, and albumin, are critically assessed. While experimental studies have provided preliminary evidence supporting HBP-targeted intervention, clinical validation in transplant populations remains insufficient. Future studies should define the temporal dynamics, cellular sources, and context-specific effects of HBP after transplantation. Collectively, available evidence indicates that HBP may serve as a potential biomarker and therapeutic target, but its clinical application requires further validation through mechanistic and prospective studies.