Interleukin-17 receptor polymorphism predisposes to primary graft dysfunction after lung transplantation

Abstract

Both genetic variants of IL-17R (rs882643 and rs2241049) were associated with PGD. This confirms a genetic predisposition toward PGD and suggests a role of IL-17 in driving neutrophilia in PGD.

Report of the ISHLT Working Group on Primary Lung Graft Dysfunction Part III: Mechanisms: A 2016 Consensus Group Statement of the International Society for Heart and Lung Transplantation

“…Consistent with these observations were reports showing that having either elevated RAGE plasma levels or carrying certain IL-17 receptor polymorphisms increased the risk for PGD. 10,41 …”

Cell-free hemoglobin promotes primary graft dysfunction through oxidative lung endothelial injury

“…A variety of clinical risk factors for PGD have been identified with contributions from the donor (3)(4)(5)(6)(7), the recipient (3)(4)(5)(7)(8)(9)(10), and operative variables (4,5,8,11). In addition, a number of biomarkers have been associated with increased risk of PGD, including markers of innate and adaptive immune activation, epithelial and endothelial injury, coagulation, vascular permeability, and lipid peroxidation (2,(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27). Despite identification of these clinical and biomarker predictors of PGD, the mechanisms leading to PGD are not well understood, and there are no specific therapeutic interventions for PGD.…”

Immediate post‐operative broncho‐alveolar lavage IL‐6 and IL‐8 are associated with early outcomes after lung transplantation

“…The list of involved proteins and genes is extensive and includes IL‐6, IL‐8, pentraxin 3, TLR4, receptor for advanced glycation end (RAGE) products and VEGF, amongst others . Some patients also seem to be more prone to develop PGD, as evidenced by sequencing recipient single nucleotide polymorphisms for pentraxin 3, IL‐17A, and prostaglandin …”