Allan Tsung

University of Pittsburgh, Pittsburgh, Pennsylvania, United States

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Publications (141)639.64 Total impact

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    ABSTRACT: Laparoscopic liver resection (LLR) for metastatic colorectal cancer (mCRC) remains controversial. The objective of this manuscript was to perform a metaanalysis comparing outcomes of LLR with open liver resection (OLR) in patients with hepatic mCRC, and to identify which patients were suitable candidates for LLR.
    Surgery 10/2014; · 3.37 Impact Factor
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    ABSTRACT: Previous studies have reported that an elevated preoperative Neutrophil-Lymphocyte Ratio (NLR) is associated with poor prognosis in patients with various solid tumors including colorectal cancer (CRC). Here, we examine whether NLR predicts survival in patients with unresectable CRC metastases undergoing hepatic radioembolization.
    Annals of Surgical Oncology 09/2014; · 4.12 Impact Factor
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    ABSTRACT: AimTo evaluate the outcomes among elderly (≥70 years) and younger patients (<70 years) with liver-dominant metastatic colorectal cancer (mCRC) who received radioembolization (RE) as salvage therapy.MethodsA retrospective review of 107 consecutive patients with unresectable mCRC treated with RE after failing first- and second-line chemotherapy.ResultsFrom 2002 to 2012, 44 elderly and 63 younger (<70 years) patients received RE. Patients had similar previous extensive chemotherapy and liver-directed interventions. Using modified Response Evaluation Criteria in Solid Tumors (mRECIST) criteria, either a stable or a partial radiographical response was seen in 65.8% of the younger compared with 76.5% of the elderly patients. RE was equally well tolerated in both groups and common procedure-related adverse events were predominantly grade 1–2 and of short duration. No significant difference was found with regard to overall median survival between younger [8.4 months; 95% confidence interval (CI) = 6.2–10.6] or elderly patients (8.2 months; 95% CI = 5.9–10.5, P = 0.667). The presence of extrahepatic disease at the time of RE was associated with a significantly worse median survival in both groups.Conclusion Radioembolization appears to be as well tolerated and effective for the elderly as it is for younger patients with mCRC. Age alone should not be a discriminating factor for the use of radioembolization in the management of mCRC patients.
    HPB 09/2014; · 1.94 Impact Factor
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    ABSTRACT: BACKGROUND Evidence continues to accumulate regarding the association between health-related quality of life (HRQoL) and survival across chronic diseases. The objectives of the current study were to investigate the prognostic value of HRQoL in patients with hepatocellular carcinoma and cholangiocarcinoma after adjusting for sociodemographics, disease-related factors, and treatment-related factors.METHODSA total of 321 patients diagnosed with hepatocellular or cholangiocarcinoma were administered the Functional Assessment of Cancer Therapy-Hepatobiliary instrument. Cox regression and Kaplan-Meier survival analyses were performed to test the association between the 5 domains of HRQoL and survival.RESULTSUsing Cox regression, overall HRQoL was found to be significantly associated with survival (P = .003) after adjusting for demographics, disease-specific factors, and treatment. Subscales of the Functional Assessment of Cancer Therapy-Hepatobiliary, including the Physical Well-Being (P = .02) and the Symptoms and Side Effects subscales (P = .05), were also found to be significantly associated with survival after adjusting for demographics, disease-specific factors, and treatment.CONCLUSIONSHRQoL was found to be prognostic of survival in patients with hepatocellular and cholangiocarcinoma while covarying for demographics, disease-specific factors, and treatment. Stratifying patients based on HRQoL when testing novel treatments may be recommended.Health-related quality of life was found to be prognostic of survival in patients with hepatocellular and cholangiocarcinoma while controlling for demographics, disease-specific factors, and treatment-related factors. Cancer 2014. © 2014 American Cancer Society.
    Cancer 08/2014; · 5.20 Impact Factor
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    ABSTRACT: Complex genetic and physiological variations as well as environmental factors that drive emergence of chromosomal instability, development of unscheduled cell death, skewed differentiation, and altered metabolism are central to the pathogenesis of human diseases and disorders. Understanding the molecular bases for these processes is important for the development of new diagnostic biomarkers, and for identifying new therapeutic targets. In 1973, a group of non-histone nuclear proteins with high electrophoretic mobility was discovered and termed High-Mobility Group (HMG) proteins. The HMG proteins include three superfamilies termed HMGB, HMGN, and HMGA. High-mobility group box 1 (HMGB1), the most abundant and well-studied HMG protein, senses and coordinates the cellular stress response and plays a critical role not only inside of the cell as a DNA chaperone, chromosome guardian, autophagy sustainer, and protector from apoptotic cell death, but also outside the cell as the prototypic damage associated molecular pattern molecule (DAMP). This DAMP, in conjunction with other factors, thus has cytokine, chemokine, and growth factor activity, orchestrating the inflammatory and immune response. All of these characteristics make HMGB1 a critical molecular target in multiple human diseases including infectious diseases, ischemia, immune disorders, neurodegenerative diseases, metabolic disorders, and cancer. Indeed, a number of emergent strategies have been used to inhibit HMGB1 expression, release, and activity in vitro and in vivo. These include antibodies, peptide inhbitiors, RNAi, anti-coagulants, endogenous hormones, various chemical compounds, HMGB1-receptor and signaling pathway inhibition, artificial DNAs, physical strategies including vagus nerve stimulation and other surgical approaches. Future work further investigating the details of HMGB1 localizationtion, structure, post-translational modification, and identifccation of additional partners will undoubtedly uncover additional secrets regarding HMGB1's multiple functions.
    Molecular Aspects of Medicine 07/2014; · 10.38 Impact Factor
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    ABSTRACT: The management of hepatic hemangiomas remains ill defined. This study sought to investigate the indications, surgical management and outcomes of patients who underwent a resection for hepatic hemangiomas.
    HPB 06/2014; · 1.94 Impact Factor
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    ABSTRACT: Purpose: Management guidelines for pancreatic IPMNs and MCNs are based on the assumption that mucinous cysts can be accurately distinguished from other pancreatic cystic lesions. Previous studies using surgical material have identified recurrent mutations in GNAS and KRAS in pancreatic mucinous neoplasms. Yet, the diagnostic utility of testing for both genes in pancreatic cyst fluid obtained by endoscopic ultrasound-fine needle aspiration (EUS-FNA) remains unclear. Experimental Design: GNAS and KRAS testing was performed on EUS-FNA obtained fluid from 91 pancreatic cysts: 41 IPMNs, 9 IPMNs with adenocarcinoma, 16 MCNs, 10 cystic pancreatic neuroendocrine tumors (PanNETs), 9 serous cystadenomas (SCA), 3 retention cysts, 2 pseudocysts and 1 lymphoepithelial cyst. Results: Mutations in GNAS were detected in 16 (39%) IPMNs and 2 (22%) IPMNs with adenocarcinoma. KRAS mutations were identified in 28 (68%) IPMNs, 7 (78%) IPMNs with adenocarcinoma, and 1 (6%) MCN. Mutations in either gene were present in 34 (83%) IPMNs, 8 (89%) IPMNs with adenocarcinoma, and 1 (6%) MCN. No mutations were found in cystic PanNETs, SCAs, retention cysts, pseudocysts and a lymphoepithelial cyst. GNAS and KRAS mutations had 100% specificity (95% confidence interval [CI], 0.83-1.00), but 65% sensitivity (95% CI, 0.52-0.76) for mucinous differentiation. Among IPMNs, mutations in either gene had a 98% specificity (95% CI, 0.86-1.00) and 84% sensitivity (95% CI, 0.70-0.92). Conclusions: The combination of GNAS and KRAS testing was highly specific and sensitive for IPMNs; however, the lack of sensitivity for MCNs highlights the need for additional markers to improve the detection of pancreatic mucinous neoplasms.
    Clinical cancer research : an official journal of the American Association for Cancer Research. 06/2014;
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    ABSTRACT: High mobility group box 1 (HMGB1) was originally defined as a ubiquitous nuclear protein, but it was later determined that the protein has different roles both inside and outside of cells. Nuclear HMGB1 regulates chromatin structure and gene transcription, whereas cytosolic HMGB1 is involved in inflammasome activation and autophagy. Extracellular HMGB1 has drawn attention because it can bind to related cell signalling transduction receptors, such as the receptor for advanced glycation end-products, toll-like receptor (TLR)2, TLR4 and TLR9. It also participates in the development and progression of a variety of diseases. HMGB1 is actively secreted by stimulation of the innate immune system, and it is passively released by ischaemia or cell injury. This review focuses on the important role of HMGB1 in the pathogenesis of acute and chronic sterile inflammatory conditions. Strategies that target HMGB1 have been shown to significantly decrease inflammation in several disease models of sterile inflammation, and this may represent a promising clinical approach for treatment of certain conditions associated with sterile inflammation. This article is protected by copyright. All rights reserved.
    Journal of Internal Medicine 06/2014; · 6.46 Impact Factor
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    ABSTRACT: Background and Rationale. Acetaminophen (APAP) toxicity is the most common cause of acute liver failure in industrialized countries. Understanding the mechanisms of APAP-induced liver injury as well as other forms of sterile liver injury is critical to improve the care of patients. Recent studies demonstrate that danger signaling and inflammasome activation play a role in APAP-induced injury. The purpose of these investigations was to test the hypothesis that benzyl alcohol (BA) is a therapeutic that protects against APAP-induced liver injury via modulation of danger signaling. Main Results. APAP-induced liver injury was dependent in part on TLR-9 and receptor for advanced glycation endproducts (RAGE) signaling. BA limited liver injury over a dose range of 135-540 µg/g body weight or when delivered as a pre-, concurrent, or post-APAP therapeutic. Furthermore, BA abrogated APAP-induced cytokines and chemokines as well as high mobility group box-1 release. Moreover, BA prevented APAP-induced inflammasome signaling as determined by IL-1β, IL-18 and caspase-1 cleavage in liver tissues. Interestingly, the protective effects of BA on limiting liver injury and inflammasome activation were dependent on TLR4 signaling, but not TLR2 or Cluster of differentiation 14 (CD14). Cell type specific knockouts of TLR4 were utilized in order to further determine the protective mechanisms of BA. These studies found that TLR4 expression specifically in myeloid cells (LyzCre-tlr4-/-) were necessary for the protective effects of BA. Conclusion: BA protects against APAP-induced acute liver injury and reduced inflammasome activation in a TLR4-dependent manner. BA may prove to be a useful adjunct in the treatment of APAP and other forms of sterile liver injury. (Hepatology 2014)
    Hepatology 05/2014; · 12.00 Impact Factor
  • Allan Tsung, David A Geller
    Annals of surgery 04/2014; · 7.90 Impact Factor
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    ABSTRACT: Prior liver transplantation and immunosuppression potentially translate into significant morbidity and poor outcomes after any type of pancreatic surgery. Little is known about the outcomes of pancreatic surgery after liver transplantation. This study was designed to review our experience regarding the indications and outcomes of pancreatic surgery following liver transplantation. A retrospective review of all liver transplant recipients who underwent pancreatic surgery between 1991 and 2009 was performed. A total of 3196 patients underwent liver transplantation, of whom 18 (0.6%) subsequently required pancreatic surgery. The most common indications were necrotizing pancreatitis and lesions of the head and tail of the pancreas. Procedures performed included pancreaticoduodenectomy, distal pancreatectomy, and pancreatic necrosectomy. The estimated blood loss was 500 mL and operative time was 430 ± 224 min. Pathology results revealed malignant lesions in six (33%) patients, pre-malignant lesions in 2 (11%) patients, and benign lesions in 10 (56%) patients. The median time from transplantation to pancreatic surgery was 61 months. The 30-d postoperative complication rate was 77.8%, with median hospital stay of 15 d. The three-, 12-, and 24-month survival rates were 78%, 48%, and 24%, respectively. Pancreatic surgery after liver transplantation results in significant 30-d complications. Prior liver transplantation, however, should not be a contraindication for subsequent pancreatic surgery, due to its decent survival outcome.
    Clinical Transplantation 03/2014; 28(3):330-6. · 1.63 Impact Factor
  • Journal of Surgical Research 02/2014; 186(2):494. · 2.02 Impact Factor
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    ABSTRACT: We sought to identify a secreted biomarker for β-catenin activation commonly seen in hepatocellular carcinoma (HCC). By examination of our previously published genearray of hepatocyte-specific β-catenin knockout (KO) livers, we identified secreted factors whose expression may be β-catenin-dependent. We verified expression and secretion of the leading factor in HCC cells transfected with mutated (Hep3BS33Y)-β-catenin. Serum levels of biomarker were next investigated in a mouse model of HCC with β-catenin gene (Ctnnb1) mutations and eventually in HCC patients. Leukocyte cell-derived chemotaxin-2 (LECT2) expression was decreased in KO livers. Hep3BS33Y expressed and secreted more LECT2 in media as compared to Hep3BWT. Mice developing HCC with Ctnnb1 mutations showed significantly higher serum LECT2 levels. However patients with CTNNB1 mutations showed LECT2 levels of 54.28±22.32 ng/mL (Mean ± SD; n = 8) that were insignificantly different from patients with non-neoplastic chronic liver disease (32.8±21.1 ng/mL; n = 15) or healthy volunteers (33.2±7.2 ng/mL; n = 11). Intriguingly, patients without β-catenin mutations showed significantly higher serum LECT2 levels (54.26 ± 22.25 ng/mL; n = 46). While β-catenin activation was evident in a subset of non-mutant β-catenin HCC group with high LECT2 expression, serum LECT2 was unequivocally similar between β-catenin-active and -normal group. Further analysis showed that LECT2 levels greater than 50 ng/ml diagnosed HCC in patients irrespective of β-catenin mutations with specificity of 96.1% and positive predictive value of 97.0%. Thus, LECT2 is regulated by β-catenin in HCC in both mice and men, but serum LECT2 reflects β-catenin activity only in mice. Serum LECT2 could be a potential biomarker of HCC in patients.
    PLoS ONE 01/2014; 9(6):e98817. · 3.53 Impact Factor
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    ABSTRACT: High mobility group box-1 (HMGB1) is an abundant chromatin associated nuclear protein and released into the extracellular milieu during liver ischemia/reperfusion (I/R), signaling the activation of pro-inflammatory cascades. Since the intracellular function of HMGB1 during the sterile inflammation of I/R is currently unknown, we sought to determine the role of intracellular HMGB1 in hepatocytes following liver I/R. When hepatocyte specific HMGB1 knockout (HMGB1-HC-KO) and control mice were subjected to a non-lethal warm liver I/R, it was found that HMGB1-HC-KO mice had significantly greater hepatocellular injury after I/R compared to control mice. Additionally, there was significantly greater DNA damage and decreased chromatin accessibility to repair with lack of HMGB1. Furthermore, lack of hepatocyte HMGB1 led to excessive poly (ADP-ribose) polymerase-1 (PARP-1) activation, exhausting NAD(+) and ATP stores, exacerbating mitochondrial instability and damage, and consequently leading to increased cell death. We found that this was also associated with significantly more oxidative stress in HMGB1-HC-KO mice compared to control. Increased nuclear instability led to a resultant increase in the release of histones with subsequently more inflammatory cytokine production and organ damage through the activation of TLR9. Conclusion: Therefore, the lack of HMGB1 within hepatocytes leads to the increased susceptibility to cellular death after oxidative stress conditions. (Hepatology 2013;).
    Hepatology 12/2013; · 12.00 Impact Factor
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    ABSTRACT: & Aims: High mobility group box 1 (HMGB1) is an abundant protein that regulates chromosome architecture and also functions as a damage-associated molecular pattern molecule. Little is known about its intracellular roles in response to tissue injury or during subsequent local and systemic inflammatory responses. We investigated the function of Hmgb1 in mice following induction of acute pancreatitis. We utilized a Cre/LoxP system to create mice with pancreas-specific disruption in Hmbg1 (Pdx1-Cre; HMGB1flox/flox mice). Acute pancreatitis was induced in these mice (HMGB1flox/flox mice served as controls) following injection of L-arginine or cerulein. Pancreatic tissues and acinar cells were collected and analyzed by histologic, immunoblot, and immunohistochemical analyses. Following injection of L-arginine or cerulein, Pdx1-Cre; HMGB1flox/flox mice developed acute pancreatitis more rapidly than controls, with increased mortality. Pancreatic tissues of these mice also had higher levels of serum amylase, acinar cell death, leukocyte infiltration, and interstitial edema than controls. Pancreatic tissues and acinar cells collected from the Pdx1-Cre; HMGB1flox/flox mice following L-arginine- or cerulein injection demonstrated nuclear catastrophe with greater nucleosome release when compared with controls, along with increased phosphorylation/activation of RELA Nfκb, degradation of Iκb, and phosphorylation of Mapk. Inhibitors of reactive oxygen species (N-acetyl-L-cysteine) blocked L-arginine-induced DNA damage, necrosis, apoptosis, release of nucleosomes, and activation of Nfκb in pancreatic tissues and acinar cells from Pdx1-Cre; HMGB1flox/flox and control mice. Exogenous genomic DNA and recombinant histone H3 proteins significantly induced release of HMGB1 from mouse macrophages; administration of antibodies against H3 to mice reduced serum levels of HMGB1 and increased survival following L-arginine injection. In 2 mouse models of acute pancreatitis, intracellular HMGB1 appeared to prevent nuclear catastrophe and release of inflammatory nucleosomes to block inflammation. These findings indicate a role for the innate immune response in tissue damage.
    Gastroenterology 12/2013; · 12.82 Impact Factor
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    ABSTRACT: To evaluate our experience with the use of yttrium-90 ((90)Y) radioembolization in maintaining potential candidacy and, in some instances, downstaging hepatocellular carcinoma (HCC) that does not meet Milan criteria for liver transplantation. A retrospective review of 20 consecutive patients with HCC who were listed to receive a liver transplant and were treated with (90)Y radioembolization as a sole modality for locoregional "bridge" therapy was performed. Demographics, radiographic and pathologic response, survival, and recurrences were examined. Twenty-two (90)Y treatments were performed in 20 patients before transplantation. Median time from first treatment to transplantation was 3.5 months. HCC in 14 patients met the Milan criteria at the time of the first (90)Y treatment, and HCC in six did not. All cases that originally met the Milan criteria remained within the criteria before transplantation, and two of six patients whose disease did not meet the criteria (33%) had their disease successfully downstaged to meet the criteria. Overall, nine patients (45%) had complete or partial radiologic response to (90)Y radioembolization according to modified Response Evaluation Criteria In Solid Tumors. Complete necrosis of tumor with no evidence of viable tumor on pathologic examination was observed in five patients (36%) whose disease met the Milan criteria. Particularly in regions with long wait list times, (90)Y treatment is effective in maintaining tumor size in potential liver transplantation candidates with HCC. In addition, it can also be considered as a downstaging therapy in select patients before transplantation.
    Journal of vascular and interventional radiology: JVIR 11/2013; 24(11):1632-8. · 1.81 Impact Factor
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    ABSTRACT: To perform a matched comparison of surgical and postsurgical outcomes between our robotic and laparoscopic hepatic resection experience. The application of robotic technology and technique to liver surgery has grown. Robotic methods may have the potential to overcome certain laparoscopic disadvantages, but few studies have drawn a matched comparison of outcomes between robotic and laparoscopic liver resections. Demographics, intraoperative variables, and postoperative outcomes among patients undergoing robotic (n = 57) and laparoscopic (n = 114) hepatic resections between November 2007 and December 2011 were reviewed. A 1:2 matched analysis was performed by individually matching patients in the robotic cohort to patients in the laparoscopic cohort based on demographics, comorbidities, performance status, and extent of liver resection. Matched patients undergoing robotic and laparoscopic liver resections displayed no significant differences in operative and postoperative outcomes as measured by blood loss, transfusion rate, R0 negative margin rate, postoperative peak bilirubin, postoperative intensive care unit admission rate, length of stay, and 90-day mortality. Patients undergoing robotic liver surgery had significantly longer operative times (median: 253 vs 199 minutes) and overall room times (median: 342 vs 262 minutes) compared with their laparoscopic counterparts. However, the robotic approach allowed for an increased percentage of major hepatectomies to be performed in a purely minimally invasive fashion (81% vs 7.1%, P < 0.05). This is the largest series comparing robotic to laparoscopic liver resections. Robotic and laparoscopic liver resection display similar safety and feasibility for hepatectomies. Although a greater proportion of robotic cases were completed in a totally minimally invasive manner, there were no significant benefits over laparoscopic techniques in operative outcomes.
    Annals of surgery 09/2013; · 7.90 Impact Factor
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    ABSTRACT: Cellular processes that drive sterile inflammatory injury after hepatic ischemia/reperfusion (I/R) injury are not completely understood. Activation of the inflammasome plays a key role in response to invading intracellular pathogens, but mounting evidence suggests that it also plays a role in inflammation driven by endogenous danger-associate molecular pattern molecules released after ischemic injury. The nucleotide-binding domain, leucine-rich repeat containing protein 3 (NLRP3) inflammasome is one such process, and the mechanism by which its activation results in damage and inflammatory responses following liver I/R is unknown. In this article, we report that both NLRP3 and its downstream target caspase-1 are activated during I/R and are essential for hepatic I/R injury, because both NLRP3 and caspase-1 knockout mice are protected from injury. Furthermore, inflammasome-mediated injury is dependent on caspase-1 expression in liver nonparenchymal cells. Although upstream signals that activate the inflammasome during ischemic injury are not well characterized, we show that endogenous extracellular histones activate the NLRP3 inflammasome during liver I/R through TLR9. This occurs through TLR9-dependent generation of reactive oxygen species. This mechanism is operant in resident liver Kupffer cells, which drive innate immune responses after I/R injury by recruiting additional cell types, including neutrophils and inflammatory monocytes. These novel findings illustrate a new mechanism by which extracellular histones and activation of NLRP3 inflammasome contribute to liver damage and the activation of innate immunity during sterile inflammation.
    The Journal of Immunology 07/2013; · 5.52 Impact Factor
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    ABSTRACT: Autophagy has emerged as a critical lysosomal pathway that maintains cell function and survival through the degradation of cellular components such as organelles and proteins. Investigations specifically employing the liver or hepatocytes as experimental models have contributed significantly to our current knowledge of autophagic regulation and function. The diverse cellular functions of autophagy, along with unique features of the liver and its principal cell type the hepatocyte, suggest that the liver is highly dependent on autophagy for both normal function and to prevent the development of disease states. However, instances have also been identified in which autophagy promotes pathological changes such as the development of hepatic fibrosis. Considerable evidence has accumulated that alterations in autophagy are an underlying mechanism of a number of common hepatic diseases including toxin-, drug- and ischemia/reperfusion-induced liver injury, fatty liver, viral hepatitis and hepatocellular carcinoma. This review summarizes recent advances in understanding the roles that autophagy plays in normal hepatic physiology and pathophysiology with the intent of furthering the development of autophagy-based therapies for human liver diseases.
    Autophagy 05/2013; 9(8). · 12.04 Impact Factor
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    ABSTRACT: Ischemia-reperfusion (I/R) injury is a process whereby an initial hypoxic insult and subsequent return of blood flow leads to the propagation of innate immune responses and organ injury. The necessity of the pattern recognition receptor, toll-like receptor (TLR)-4, for this innate immune response has been previously shown. However, TLR4 is present on various cell types of the liver, both immune and non-immune cells. Therefore, we sought to determine the role of TLR4 in individual cell populations, specifically parenchymal hepatocytes, myeloid cells including Kupffer cells, and dendritic cells following hepatic I/R. When hepatocyte specific (Alb-TLR4-/- ) and myeloid cell specific (Lyz-TLR4-/- ) TLR4 knockout mice were subjected to warm hepatic ischemia there was significant protection in these mice compared to wild-type (WT). However, the protection afforded in these two strains was significantly less than global TLR4 knockout (TLR4-/- ) mice. Dendritic cell specific TLR4-/- (CD11c-TLR4-/- ) mice had significantly increased hepatocellular damage compared to WT mice. Circulating levels of high mobility group box-1 (HMGB1) were significantly reduced in the Alb-TLR4-/- mice compared to WT, Lyz-TLR4-/- , CD11c-TLR4-/- mice and equivalent to global TLR4-/- mice, suggesting that TLR4 mediated HMGB1 release from hepatocytes may be a source of HMGB1 after I/R. Hepatocytes exposed to hypoxia responded by rapidly phosphorylating the mitogen-activated protein kinases JNK and p38 in a TLR4-dependent manner; inhibition of JNK decreased the release of HMGB1 after both hypoxia in vitro and I/R in vivo. Conclusion: These results provide insight into the individual cellular response of TLR4. It was found that the parenchymal hepatocyte is an active participant in the sterile inflammatory response after I/R through TLR4-mediated activation of pro-inflammatory signaling and release of danger signals such as HMGB1. (HEPATOLOGY 2013.).
    Hepatology 03/2013; · 12.00 Impact Factor

Publication Stats

4k Citations
639.64 Total Impact Points

Institutions

  • 2007–2014
    • University of Pittsburgh
      • • Division of Hepato-Pancreato-Biliary (HPB) Surgery
      • • Department of Surgery
      Pittsburgh, Pennsylvania, United States
  • 2013
    • Central South University
      Ch’ang-sha-shih, Hunan, China
    • University of Maryland Medical Center
      Baltimore, Maryland, United States
  • 2012
    • University of Michigan
      • Life Sciences Institute
      Ann Arbor, MI, United States
    • Medical College of Wisconsin
      • Division of Surgical Oncology
      Milwaukee, WI, United States
    • Tongji Hospital
      Wu-han-shih, Hubei, China
    • Montefiore Medical Center
      New York City, New York, United States
  • 2010
    • McGill University
      • Department of Surgery
      Montréal, Quebec, Canada