Xing S.,Huazhong University of Science and Technology |
Xing S.,Key Laboratory of Organ Transplantation |
Li Z.-W.,Huazhong University of Science and Technology |
Tian Y.-F.,Huazhong University of Science and Technology |
And 6 more authors.
Hepatobiliary and Pancreatic Diseases International | Year: 2013
Background: Several reports have inconsistently demonstrated that there is an association between hepatitis B virus (HBV) or hepatitis C virus (HCV) infections and pancreatic cancer (PC). The aim of the present meta-analysis is to assess this possible relationship. DATA SOURCES: Studies were identified by searching available database from January 2000 to July 2012. Possible associations between PC risk and hepatitis B surface antigen (HBsAg) and its antibody (HBsAb), hepatitis B e antigen (HBeAg) and its antibody (HBeAb), anti-HBcAg antibody (HBcAb), and HCV antibody (anti-HCV) were evaluated. Results: Eight case-control and two cohort studies were included, and their quality scores were assessed by the modified Newcastle-Ottawa Quality Assessment Scale (NOS). We found that HBsAg and anti-HCV seropositivity significantly increased risk of PC (OR=1.28, 95% CI: 1.11-1.48 and OR=1.21, 95% CI: 1.02-1.44). The presence of HBsAb was associated with a statistically significant decrease in the risk of PC (OR=0.40, 95% CI: 0.20-0.79) and HBeAb (OR=0.62, 95% CI: 0.39-0.99). HBsAg-/HBcAb+/HBsAb- or HBsAg-/HBcAb+/HBsAb+ profile was not related to PC risk (OR=1.57, 95% CI: 0.83-2.98 and OR=1.24, 95% CI: 0.72-2.14). Conclusions: HBV/HCV infection increases the risk of PC. HBsAb and HBeAb seropositivity may be the protective factors against PC. It is still uncertain whether serological pattern of past exposure to HBV with or without natural immunity is associated with an enhanced probability of this malignancy. © 2013, Hepatobiliary Pancreat Dis Int. All rights reserved.
Chen G.,Huazhong University of Science and Technology |
Chen G.,Key Laboratory of Organ Transplantation |
Chen S.,Huazhong University of Science and Technology |
Chen S.,Key Laboratory of Organ Transplantation |
And 2 more authors.
Immunobiology | Year: 2013
The complement cascade is a major contributor to the innate immune response. It has now been well accepted that complement plays a critical role in hyperacute rejection and acute antibody-mediated rejection of transplanted organ. There is also increasing evidence that complement proteins contribute to the pathogenesis of organ ischemia-reperfusion injury, and even to cell-mediated rejection. Furthermore, the chemoattractants C3a and C5a and the terminal membrane attack complex that are generated by complement activation can directly or indirectly mediate tissue injury and trigger adaptive immune responses. Here, we review recent findings concerning the role of complement in graft ischemia-reperfusion injury, antibody-mediated rejection and accommodation, and cell-mediated rejection. We also discuss the current status of complement intervention therapies in clinical transplantation and describe potential new therapeutic strategies for clinical application. © 2012 Elsevier GmbH.
Wang S.F.,Key Laboratory of Organ Transplantation |
Huang Z.Y.,Key Laboratory of Organ Transplantation |
Chen X.P.,Key Laboratory of Organ Transplantation
Liver Transplantation | Year: 2011
Biliary complications occur more frequently after living donor liver transplantation (LDLT) versus deceased donor liver transplantation, and they remain the most common and intractable problems after LDLT. The anatomical limitations of multiple tiny bile ducts and the differential blood supplies of the graft ducts may be significant factors in the pathophysiological mechanisms of biliary complications in patients undergoing LDLT. A clear understanding of the biliary blood supply, the Glissonian sheath, and the hilar plate has contributed to new techniques for preparing bile ducts for anastomosis, and these techniques have resulted in a dramatic drop in the incidence of biliary complications. Most biliary complications after LDLT can be successfully treated with nonsurgical approaches, although the management of multiple biliary anastomoses and nonanastomotic strictures continues to be a challenge. © 2011 AASLD.
Zhang W.,Huazhong University of Science and Technology |
Huang Z.-Y.,Huazhong University of Science and Technology |
Ke C.-S.,Huazhong University of Science and Technology |
Wu C.,Huazhong University of Science and Technology |
And 7 more authors.
Medicine (United States) | Year: 2015
The ideal surgical treatment of giant liver hemangioma is still controversial. This study aims to compare the outcomes of enucleation with those of resection for liver hemangioma larger than 10cm in different locations of the liver and establish the preoperative predictors of increased intraoperative blood loss. Eighty-six patients underwent enucleation or liver resection for liver hemangioma larger than 10cm was retrospectively reviewed. Patient demographic, tumor characteristics, surgical indications, the outcomes of both surgical treatment, and the clinicopathological parameters influencing intraoperative blood loss were analyzed. Forty-six patients received enucleation and 40 patients received liver resection. Mean tumor size was 14.1cm with a range of 10-35cm. Blood loss, blood product usage, operative time, hepatic vascular occlusion time and frequency, complications and postsurgical hospital stay were similar between liver resections and enucleation for right-liver and left-liver hemangiomas. There was no surgery-related mortality in either group. Bleeding was more related to adjacency of major vascular structures than the size of hemangioma. Adjacency to major vascular structures and right or bilateral liver hemangiomas were independently associated with blood loss >550mL (P=0.000 and 0.042, respectively). Both enucleation and liver resection are safe and effective surgical treatments for liver hemangiomas larger than 10cm. The risk of intraoperative blood loss is related to adjacency to major vascular structures and the location of hemangioma. © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Ruan Y.,Huazhong University of Science and Technology |
Wang L.,Huazhong University of Science and Technology |
Zhao Y.,Huazhong University of Science and Technology |
Yao Y.,Huazhong University of Science and Technology |
And 9 more authors.
Kidney International | Year: 2014
High-mobility group box 1 (HMGB1) is a chromatin-binding nuclear molecule that has potent proinflammatory effects once released by damaged cells. In some disease models, carbon monoxide (CO) exhibits anti-inflammatory and protective properties. Here, we investigated whether the protective effect of CO on renal ischemia-reperfusion injury is associated with the inhibition of HMGB1 translocation and release. A renal ischemia-reperfusion injury model was established with a 100% mortality rate in untreated mice. Pretreatment with the CO-releasing molecule-2 (CORM-2) resulted in 100% survival, maximal preservation of renal function, a marked reduction in pathological damage, and blunted upregulation of TLR4, RAGE, TNF-α, IL-1Β, IL-6, and MCP1 mRNA. Interestingly, CORM-2 pretreatment almost completely inhibited ischemia-induced HMGB1 nucleocytoplasmic shuttling and release. This inhibition was associated with a decrease in nuclear histone acetyltransferase activity. Indeed, CORM-2 pretreatment inhibited the acetylation and release of HMGB1 during hypoxic culture of primary mouse renal tubular epithelia cells in vitro. Using the same renal ischemia-reperfusion injury model, neutralization of HMGB1 was protective, and administration of exogenous HMGB1 largely reversed the protective effect of CORM-2 on kidney ischemia-reperfusion injury. Thus, CORM-2-delivered CO protects against lethal renal ischemia-reperfusion injury. This protection is correlated with the prevention of HMGB1 nuclear-cytoplasmic translocation and release. © 2014 International Society of Nephrology.
Xu Q.,Huazhong University of Science and Technology |
Zheng F.,Huazhong University of Science and Technology |
Gong F.,Huazhong University of Science and Technology |
Gong F.,Key Laboratory of Organ Transplantation |
And 2 more authors.
Journal of Gene Medicine | Year: 2014
Background: Suppressor of cytokine signaling 3 (SOCS3) is the main negative feedback regulator of cytokine signals. We investigated the hypothesis that overexpression of SOCS3 in a murine cardiac allograft transplantation model may result in a survival advantage of the allograft by attenuating alloreactive T-cell responses. Methods: With the use of BALB/c (H-2d) donor mice and C57Bl/6j (H-2b) recipient mice, the murine cardiac transplantation model was established. Recipient mice received a tail intravenous injection with eukaryotic expression plasmid pEF-FLAG-I/mSOCS3 before and after transplantation. The heart beat of the grafts and immune responses were monitored. Results: Overexpression of SOCS3 within grafts and spleens can prolong the survival time of cardiac allografts by attenuating infiltration of inflammatory cells such as T cells and macrophages in the grafts, decreasing the number of CD4+IL-17+ cells and CD8+IL-17+ cells in spleens, as well as reducing the expression of STAT3 in grafts and phosphorylation of STAT3 in both grafts and spleens. Conclusions: Overexpression of SOCS3 significantly delays cardiac allograft acute rejection, which is associated with reduced allograft proinflammatory leukocyte infiltration and impaired alloreactive IL-17+ T cell immunity. © 2014 John Wiley & Sons, Ltd.
Liu L.-P.,Huazhong University of Science and Technology |
Liu L.-P.,Wuhan Women and Children Medical Healthcare Center |
Huang W.,Huazhong University of Science and Technology |
Huang W.,Key Laboratory of Organ Transplantation |
And 2 more authors.
American Journal of Reproductive Immunology | Year: 2010
Problem: The aim of this study was to evaluate how fetal monocyte activation and maternal anti-fetal antigen-specific antibody-secreting cells (ASC) affect the severity of hypertensive disorder complicating pregnancy (HDCP). Method of study: Forty-six healthy third-trimester pregnant women and 20 patients with gestational hypertension, 20 with mild pre-ecalmpsia and another 20 with severe pre-eclampsia were included in the study. Interleukin-6 (IL-6) release from cord blood monocytes was examined by intracellular cytokine staining and flow cytometric analysis. Moreover, the maternal anti-fetal antigen-specific ASC were detected by enzyme-linked immunospot assay. Results: A significantly increased percentage of IL-6-positive monocytes were detected in the cord blood of study groups compared with the controls (P < 0.01). The percentage of IL-6-positive monocytes was increased as the disease progressed (P < 0.05). There were more anti-fetal antigen-specific ASC in the study groups than those in the controls (P < 0.001). Furthermore, the anti-fetal antigen-specific ASC showed difference in gestational hypertensive and severe pre-eclamptic groups (P < 0.05). Conclusion: We conclude that the fetal monocyte activation and the increase in maternal anti-fetal antigen-specific ASC were related to the incidence and severity of HDCP. These results provide both indirect and direct evidence for the occurrence of exaggerated maternal humoral immunity against the fetal antigens in HDCP. © 2010 John Wiley & Sons A/S.
Feng Z.,Zhejiang University |
Zeng S.,Southern Medical University |
Wang Y.,Zhejiang University |
Zheng Z.,Key Laboratory of Organ Transplantation |
Chen Z.,Zhejiang University
PLoS ONE | Year: 2013
Background: While bisphosphonates (BPs) are commonly used in clinical treatment for osteoporosis, their roles on osteoporosis treatment for rheumatic patients remain unclear. We performed a meta-analysis to evaluate the efficacy of BPs on fractures prevention and bone mass preserving in rheumatic patients. Methodology/Principal Findings: We searched PubMed, EmBase, and the Cochrane Central Register of Controlled Trials for relevant literatures with a time limit of Jan. 6, 2012. All randomized clinical trials of BPs for adult rheumatic patients with a follow-up of 6 months or more were included. We calculated relative risks (RRs) for fractures and weighted mean difference (WMD) for percent change of bone mineral density (BMD). Twenty trials were included for analysis. The RR in rheumatic patients treated with BPs was 0.61 (95%CI [0.44, 0.83], P = 0.002) for vertebral fractures, and 0.49 (95%CI [0.23, 1.02], P = 0.06) for non-vertebral fractures. The WMD of BMD change in the lumbar spine was 3.72% (95%CI [2.72, 4.72], P<0.001) at 6 months, 3.67% (95%CI [2.84, 4.50], P<0.001) at 12 months, 3.64% (95%CI [2.59, 4.69], P<0.001) at 24 months, and 5.87% (95%CI [4.59, 7.15], P<0.001) at 36 months in patients using BPs, as compared with those treated with calcium, vitamin D or calcitonin. In subgroup analyses, rheumatic patients using BPs for osteoporosis prevention had greater WMD than those using BPs for treating osteoporosis at 6 months (4.53% vs. 2.73%, P = 0.05) and 12 months (4.93% vs. 2.91%, P = 0.01). Conclusions/Significance: In both short-term and middle-term, BPs can preserve bone mass and reduce the incidence of vertebral fractures in rheumatic patients, mainly for those who have GC consumption. The efficacy of BPs is better when using BPs to prevent rather than to treat osteoporosis in rheumatic patients. Copyright: © 2013 Feng et al.
Xiong A.,Huazhong University of Science and Technology |
Duan L.,Huazhong University of Science and Technology |
Chen J.,Huazhong University of Science and Technology |
Fan Z.,Huazhong University of Science and Technology |
And 6 more authors.
PLoS ONE | Year: 2012
The induction of immune tolerance is still a formidable challenge in organ transplantation. Dendritic cells (DCs) play an important role in orchestrating immune responses by either mediating protective immune responses or inducing antigen specific tolerance. Previous studies demonstrated that the fms-like tyrosine kinase 3 receptor (Flt3) and its ligand (Flt3L) play an essential role in the regulation of DC commitment and development. Here, we report a synergic effect between Flt3L and low-dose rapamycin (Rapa) in the protection of allograft rejction. It was found that Flt3L combined with Rapa significantly prolonged murine cardiac allograft survival time as compared with that of untreated recipients or recipients treated with Rapa or Flt3L alone. Mechanistic studies revealed that Flt3L combined with low-dose of Rapa induced the generation of tolerogenic DCs along with the production of CD25+ Foxp3+ regulatory T cells and IL-10 secretion. We also observed enhanced autophagy in the cardiac allograft, which could be another asset contributing to the enhanced allograft survival. All together, these data suggest that Flt3L combined with low-dose of Rapa could be an effective therapeutic approach to induce tolerance in clinical setting of transplantation. © 2012 Xiong et al.
Chen S.,Huazhong University of Science and Technology |
Zhong S.,Huazhong University of Science and Technology |
Xiang Y.,Huazhong University of Science and Technology |
Li J.-H.,Huazhong University of Science and Technology |
And 9 more authors.
American Journal of Transplantation | Year: 2011
Protection against humoral injury mediated by donor-specific antibodies (DSA), also known as accommodation, may allow for long-term allograft survival in presensitized recipients. In the present study, we determined the role of complement in renal allograft accommodation in donor skin-presensitized nonhuman primates under conventional immunosuppression. Donor skin allografts were transplanted to presensitized recipients 14 days prior to renal transplantation. Renal allografts not receiving any immunosuppressive treatment developed accelerated rejection with predominantly humoral injury, which was not prevented using conventional cyclosporine (CsA) triple therapy. Inhibition of complement activation with the Yunnan-cobra venom factor (Y-CVF) successfully prevented accelerated antibody-mediated rejection and resulted in successful accommodation and long-term renal allograft survival in most presensitized recipients. Accommodation in this model was associated with the prevention of the early antibody responses induced against donor antigens by complement inhibition. Some antiapoptotic proteins and complement regulatory proteins, including Bcl-2, CD59, CD46 and clusterin, were upregulated in the surviving renal allografts. These results suggest that the complement inhibition-based strategy may be valuable alternative in future clinical cross-match positive or ABO-incompatible transplantation. © 2011 The American Society of Transplantation and the American Society of Transplant Surgeons.