Interleukin-22 (IL-22) is a recently identified regulator of inflammation, but little is known about its role in liver transplantation. Therefore, in this study, we explored the roles and the underlying mechanisms of IL-22 in acute allograft rejection by using a rat allogeneic liver transplantation model. Results showed that allograft liver transplantation led to damage of the parent liver and to significantly increased IL-22 expression in the allograft liver and plasma of the recipient rats compared with the rats who received isografts. Moreover, the significantly increased IL-22 expression was accompanied by markedly increased level of phospho-STAT3 in the allogeneic liver tissues after transplantation. Of note, neutralization of the IL-22 protein in recipient rats significantly worsened the function of the allograft liver at 1 day post-transplantation (ischemia-reperfusion injury, IRI) but improved the function at 7 days post-transplantation (acute rejection, AR). At IRI stage, IL-22 protected liver function through the increase of anti-apoptosis and pro-regeneration cytokines. However, IL-22 led to the increase of pro-inflammation factors at AR stage, accompanied by the marked increase of the Th17 and the marked decrease of Treg cells in allograft recipient rats through modulating the expression of chemokines for different cell types, which however were reversed by in vivo IL-22 neutralization. Results indicate the dual roles of IL-22 and suggest the differential potential clinical application of IL-22 at different stage of allograft liver transplantation.
A 28-year-old man complained of intermittent irritable dry cough for 2 months with occasional bloody sputum. Positron emission tomography-computed tomography (PET-CT) suggested multiple heterogeneous soft tissue masses in the inferior lobes of both lungs, with heterogeneous increases in 18F-FDG uptake. No metabolic disorders were found in the rest of the body. CT-guided percutaneous lung puncture and biopsy and immunohistochemical study confirmed pulmonary primitive neuroectodermal tumor (PNET). PNET is characterized by small round blue cells and positive CD99 expression. After six cycles of chemotherapy with ifosfamide, dacarbazine and cisplatin, the lesions diminished substantially. At 2 months after the last cycle of chemotherapy, the patient complained of exertional dyspnea. PET-CT and echocardiogram suggested a space-occupying lesion in the right atrium. Autopsy revealed that this space-occupying lesion had the same pathomorphology and immunophenotype with pulmonary PNET, suggesting metastasis of pulmonary PNET to the right atrium. Here, we reported this rare case of pulmonary PNET metastasizing, instead of direct infiltrating or extending, into the heart.
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