HMGB1 blockade did not change the IL-17 level, but decreased the IFN-γ/IL-10 ratio. HMGB1 blockade significantly improved the fibrous occlusion in the late phase. A well-established heterotopic tracheal transplantation model was used. Highlights The effect of HMGB1 on BOS after lung transplantation is unknown. Conclusions HMGB1 may be a trigger of the BOS pathogenesis and candidate target for the treatment of the disease. HMGB1 blockade significantly suppressed the CD8 T lymphocytes infiltration and decreased the serum IFN-γ/IL-10 ratio compared with the control at Day 7. HMGB1 blockade did not change the IL-17 level, but decreased the IFN-γ/IL-10 ratio in the early phase (Days 5 and 7) and significantly improved the fibrous occlusion in the late phase (Days 14, 21, and 28). Results The HMGB1 levels in the allografts were significantly increased compared with the isografts at Day 7. Infiltrating CD8 and CD4 T lymphocytes around the allografts and serum levels of IFN-γ and IL-10 were evaluated (n = 6 Day 7). The luminal fibrous occlusion was analyzed (n = 6 Days 7, 14, 21, and 28). Protein concentrations of HMGB1, interferon-γ (IFN-γ), interleukin (IL)-10, and IL-17 were analyzed in the isografts, allografts, controls, and HMGB1-neutralizing antibody administered allografts (n = 6 Days 1, 3, 5, 7, 14, 21, and 28). Methods A murine heterotopic tracheal transplantation model was used. Abstract Background Although high-mobility group box-1 (HMGB1), which is a nuclear protein, was reported to enhance the allogeneic responses in transplantation, the effect of HMGB1 on bronchiolitis obliterans syndrome (BOS) is unknown.
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