FcGBP and VCAM-1 are ponderable biomarkers for differential diagnosis of alcoholic liver cirrhosis.

BACKGROUND/ AIMS: Early diagnosis of alcoholic liver cirrhosis (ALD) and coexisting ALD and hepatitis B virus-induced cirrhosis (ALD+HBV) is primordial for an optimal management of these conditions. However, the lack of specific noninvasive biomarkers coupled with the inaccuracy of self-reported alcohol consumption make the early diagnosis of these pathologies difficult. This study aimed to identify biomarkers to diagnose ALD and differentiate ALD+HBV from HBV. METHODS: Proteomics mass spectrometry technique was used to identify specific proteins of ALD by contrasting serums of ALD to that of healthy subjects. The accuracy of the selected proteins in diagnosing ALD and discriminating ALD+HBV from HBV was assessed in two independent cohorts using the area under the receiver operator characteristic curve (AUROC). RESULTS: 452 cirrhotic and normal subjects were enrolled in this study. The proteomic results revealed that FcGBP and VCAM-1 were the highest overexpressed proteins while comparing ALD samples to the healthy cohort. The combination of these two biomarkers had an AUROC of 0.986 (P < 0.001, sensitivity: 97.2%, specificity: 100%) in identifying ALD from the healthy cohort, and AUROC of 0.781 (P < 0.001, sensitivity: 81.8%, specificity: 77.0%) in differentiating ALD+HBV from HBV. This combination was more accurate than the combination of AST/ALT, MCV and GGT (ALD vs healthy, AUROC = 0.898; ALD+HBV vs HBV, AUROC = 0.599). The discrimination performance of this combination was further validated in another independent cohort. CONCLUSION: FcGBP and VCAM-1 are two promising biomarkers in the diagnosis of ALD and in the differentiating of ALD+HBV from HBV subjects.

Effect of alcohol on clinical complications of hepatitis virus-induced liver cirrhosis: a consecutive ten-year study.

BACKGROUND AND AIMS: Although coexisting alcohol-induced liver disease and hepatitis B or C virus-induced liver cirrhosis (ALD + HBV or ALD + HCV) has been the center of recent hepatology researches, numerous controversies still persist. This study aimed to showcase the influence of alcohol on the laboratory values and on the clinical outcomes of patients with hepatitis B and C virus-induced liver cirrhosis. METHODS: Patients diagnosed with liver cirrhosis (n = 22,287) from January 2010 to December 2019 were enrolled, and divided into five groups according to the etiology: alcohol-induced liver disease (ALD, 1652 cases), hepatitis B virus (HBV, 18,079 cases), hepatitis C virus (HCV, 682 cases), ALD + HBV (1594 cases) and ALD + HCV (280 cases). Laboratory results and proportion of different liver cirrhosis complications were contrasted between groups. RESULTS: The proportions of patients with Child Pugh grade C (28.0% vs 18.8%, P < 0.001) or MELD greater than 18 (24.1% vs 18.5%, P < 0.001) in the ALD + HBV group exceeded significantly those in the HBV group. Multivariate logistic regression revealed that the risk of hepatocellular carcinoma (HCC) and that of esophageal gastric variceal bleeding (EGVB) in the ALD + HBV group was respectively 2.01-fold and 1.74-fold that in the HBV group (HCC: OR = 2.01, 95% CI [1.58-2.55]; EGVB: OR = 1.74, 95% CI [1.30-2.33]) after adjusting for potential confounders. Furthermore, a linear-by-linear analysis test showed a decrease in the risk of HCC and EGVB with the duration of alcohol abstinence. Moreover, patients with both antiviral treatment and alcohol abstinence had the lowest risk of HCC and EGVB (HCC: OR = 0.10, 95% CI [0.05-0.20], P < 0.001; EGVB: OR = 0.17, 95% CI [0.06-0.45], P < 0.001) compared to those without any treatment, those with abstinence alone and those with antiviral therapy alone. Similar pattern was noticed while comparing the ALD + HCV group to the HCV group. CONCLUSION: Heavy alcohol use increased the severity of liver function impairment and the prevalence of HCC and EGVB in hepatitis virus-induced liver cirrhosis patients. Remarkably, long-term alcohol abstinence coupled with antiviral treatment effectively decreased the risk of HCC and EGVB in these populations.

Clinical presentation of gastric Burkitt lymphoma presenting with paraplegia and acute pancreatitis: A case report.

BACKGROUND: The incidence of gastric Burkitt lymphoma (BL), presenting as paraplegia and acute pancreatitis, is extremely low. BL is a great masquerader that presents in varied forms and in atypical locations, and it is prone to misdiagnosis and missed diagnosis. The prognosis of BL remains poor because of the difficulty in early diagnosis and the limited advances in chemotherapy. CASE SUMMARY: A 53-year-old man was referred to our hospital from the local county hospital due to abdominal pain for two weeks and weakness in the lower extremities for one day. Magnetic resonance imaging of the abdomen and lumbar spine showed a swollen pancreas and gallbladder, with peripancreatic exudation and liquid collection, indicating acute pancreatitis and acute cholecystitis. Additionally, we observed abnormally thickened lesions of the gastric wall, multiple enlarged retroperitoneal lymph nodes and a well-demarcated, posterolateral extradural mass lesion between T9 and T12, with extension through the spinal foramen and definite bony destruction, suggesting metastasis in gastric malignancy. Subsequent whole-body positron emission tomography/computed tomography examination showed multifocal malignant lesions in the stomach, pancreas, gallbladder, bone, bilateral supraclavicular fossa, anterior mediastinum, bilateral axillary and retroperitoneal lymph nodes. Gastroduodenal endoscopy revealed primary BL with massive involvement of the gastric body and duodenum. The patient refused chemotherapeutic treatment and died one week later due to upper gastrointestinal hemorrhage. Afterward, we reviewed the characteristics of 11 patients with BL involving the stomach, pancreas or spinal cord. CONCLUSION: Clinicians should be aware that BL can be the potential cause of acute pancreatitis or a rapidly progressive spinal tumor with accompanying paraplegia. For gastric BL, gastroscopy biopsies and pathology are necessary for a definite diagnosis.

Sodium butyrate protects against lipopolysaccharide-induced liver injury partially via the GPR43/ ß-arrestin-2/NF-κB network.

BACKGROUND: Butyrate acts as a regulator in multiple inflammatory organ injuries. However, the role of butyrate in acute liver injury has not yet been fully explored. In the present study, we aimed to investigate the association between butyrate and lipopolysaccharide (LPS)-induced acute liver injury and the signaling pathways involved. METHODS: LPS-induced acute liver injury was induced by intraperitoneal injection of LPS (5 mg/kg) in G-protein-coupled receptor 43 (GPR43)-knockout (KO) and wild-type female C57BL/6 mice. Sodium butyrate (500mg/kg) was administered intraperitoneally 30 min prior to LPS exposure. Liver injury was detected by serum markers, tissue morphology, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). Pro-inflammatory-factor levels were detected by enzyme-linked immunosorbent assay and real-time polymerase chain reaction (RT-PCR). Cell models were first treated with sodium butyrate (4 µmol/mL), followed by LPS (1 µg/mL) half an hour later in GPR43 small interfering RNA (siRNA)-transfected or control RAW264.7 cells. Cell-inflammation status was evaluated through detecting pro-inflammatory-factor expression by RT-PCR and also through checking toll-like receptor 4/nuclear factor-κB (TLR4/NF-κB)-element levels including TLR4, TRAF6, IKKß, IкBα, phospho-IкBα, p65, and phospho-p65 by Western blot. The interaction between GPR43 and ß-arrestin-2 was tested by co-immunoprecipitation. RESULTS: Sodium butyrate reversed the LPS-induced tissue-morphology changes and high levels of serum alanine aminotransferase, aspartate transaminase, myeloperoxidase, TUNEL, and pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin-6. The ameliorating effect of sodium butyrate was weakened in GPR43-KO mice and GPR43 siRNA RAW264.7 cells, compared with those of GPR43-positive controls. Sodium butyrate downregulated some elements of the TLR4/NF-κB pathway, including phospho-IκBα and phospho-p65, in RAW264.7 cells. Increased interactions between GPR43 and ß-arrestin-2, and between ß-arrestin-2 and IкBα were observed. CONCLUSION: Sodium butyrate significantly attenuated LPS-induced liver injury by reducing the inflammatory response partially via the GPR43/ß-arrestin-2/NF-κB signaling pathway.

Atypical Presentation of Adrenocortical Insufficiency with Anorexia and Jaundice.

BACKGROUND Adrenal insufficiency is mainly due to insufficient adrenal corticosteroid hormones secretion by the adrenal cortex, which leads to clinical manifestations such as weakness, weight loss, hyperpigmentation, hypotension, and vomiting. However, the clinical manifestations of adrenocortical insufficiency may be atypical: anorexia, ascites, impaired liver function, and alacrima have been reported. Jaundice and anorexia presenting together in the same patient as the main symptoms are rare. CASE REPORT We present a rare case of a 65-year-old woman diagnosed as having adrenocortical insufficiency with chief complaints of anorexia and jaundice. The patient had a history of hiatus hernia and gastroesophageal reflux disease, which can easily lead to a misdiagnosis in clinical practice, which is what happened with this patient at the beginning in our hospital and in the other hospitals that treated her previously. Hiatus hernia was considered the mostly likely cause of her vomiting, and a laparotomy was done to repair the hernia at the local hospital. However, there was no improvement. After regular glucocorticoid replacement, the patient's symptoms all soon disappeared. CONCLUSIONS Adrenal insufficiency can atypically present as anorexia and jaundice. In order to avoid misdiagnosis, physicians should pay attention to these atypical symptoms.

ß-arrestin 2 attenuates lipopolysaccharide-induced liver injury via inhibition of TLR4/NF-κB signaling pathway-mediated inflammation in mice.

AIM: To study the role and the possible mechanism of ß-arrestin 2 in lipopolysaccharide (LPS)-induced liver injury in vivo and in vitro. METHODS: Male ß-arrestin 2+/+ and ß-arrestin 2-/- C57BL/6J mice were used for in vivo experiments, and the mouse macrophage cell line RAW264.7 was used for in vitro experiments. The animal model was established via intraperitoneal injection of LPS or physiological sodium chloride solution. Blood samples and liver tissues were collected to analyze liver injury and levels of pro-inflammatory cytokines. Cultured cell extracts were collected to analyze the production of pro-inflammatory cytokines and expression of key molecules involved in the TLR4/NF-κB signaling pathway. RESULTS: Compared with wild-type mice, the ß-arrestin 2 knockout mice displayed more severe LPS-induced liver injury and significantly higher levels of pro-inflammatory cytokines, including interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF)-α, and IL-10. Compared with the control group, pro-inflammatory cytokines (including IL-1ß, IL-6, TNF-α, and IL-10) produced by RAW264.7 cells in the ß-arrestin 2 siRNA group were significantly increased at 6 h after treatment with LPS. Further, key molecules involved in the TLR4/NF-κB signaling pathway, including phospho-IκBα and phosho-p65, were upregulated. CONCLUSION: ß-arrestin 2 can protect liver tissue from LPS-induced injury via inhibition of TLR4/NF-κB signaling pathway-mediated inflammation.

Procedure-related complications in gastric variceal obturation with tissue glue.

AIM: To focus on procedure-related complications, evaluate their incidence, analyze the reasons and discuss the solutions. METHODS: Overall, 628 endoscopic gastric variceal obturation (EGVO) procedures (case-times) with NBC were performed in 519 patients in the Department of Endoscopy of the Third Affiliated Hospital of Sun Yat-Sen University from January 2011 to December 2016. The clinical data of patients and procedure-related complications of EGVO were retrospectively analyzed. RESULTS: In the 628 EGVO procedures, sticking of the needle to the varix occurred in 9 cases (1.43%), including 1 case that used lipiodol-diluted NBC and 8 cases that used undiluted NBC (P = 0.000). The needle was successfully withdrawn in 8 cases. Large spurt bleeding occurred in one case, and hemostasis was achieved by two other injections of undiluted glue. The injection catheter became blocked in 17 cases (2.71%) just during the injection, and 4 cases were complicated with the needle sticking to the varix. Large glue adhesion to the endoscope resulted in difficulty withdrawing the endoscope in 1 case. Bleeding from multiple sites was observed in the esophagus and gastric cardia after the endoscope was withdrawn. Hemostasis was achieved by 1% aethoxysklerol injection and intravenous somatostatin. The ligation device stuck to the varices in two cases during the subsequent endoscopic variceal ligation. In one case, the ligation device was successfully separated from the esophageal varix after all bands were released. In another case, a laceration of the vein and massive bleeding were observed. The bleeding ceased after 1% aethoxysklerol injection. CONCLUSION: Although EGVO with tissue glue is usually safe and effective, a series of complications can occur during the procedure that may puzzle endoscopists. There is no standard operating procedure for addressing these complications. The cases described in the current study can provide some reference for others.

Diagnosis of eosinophilic gastroenteritis is easily missed.

AIM: To analyze the clinical characteristics of eosinophilic gastroenteritis (EGE) and to investigate the situations of missed diagnosis of EGE. METHODS: First, the clinical characteristics of 20 EGE patients who were treated at our hospital were retrospectively summarized. Second, 159 patients who underwent gastroscopy and 211 patients who underwent colonoscopy were enrolled. The pathological diagnosis showed only chronic inflammation in their medical records. The biopsy slides of these patients were reevaluated to determine the number of infiltrating eosinophils in order to assess the probability of a missed diagnosis of EGE. Finally, 122 patients who experienced refractory upper gastrointestinal symptoms for at least one month were recruited. At least 6 biopsy specimens were obtained by gastroscopy, and the number of eosinophils that had infiltrated was evaluated. Those who met the pathological diagnostic criteria of EGE underwent further examination to confirm the diagnosis of EGE. The probability of a missed diagnosis of EGE was prospectively investigated. RESULTS: Among the 20 patients with EGE, mucosal EGE was found in 15 patients, muscular EGE was found in 3 patients and serosal EGE was found in 2 patients. Abdominal pain was the most common symptom. The number of peripheral blood eosinophils was elevated in all 20 patients, all of whom were sensitive to corticosteroids. Second, among the 159 patients who underwent gastroscopy, 7 (4.40%) patients met the criteria for pathological EGE (eosinophil count ≥ 25/HPF). Among the 211 patients who underwent colonoscopy, 9 (4.27%) patients met the criteria for pathological EGE (eosinophil count ≥ 30/HPF). No patients with eosinophil infiltration were diagnosed with EGE in clinical practice before or after endoscopy. Although these patients did not undergo further examination to exclude other diseases that can also lead to gastrointestinal eosinophil infiltration, these might be the cases where the diagnosis of EGE was missed. Finally, among the 122 patients with refractory upper gastrointestinal symptoms, eosinophil infiltration was seen in 7 patients (5.74%). The diagnosis of EGE was confirmed in all 7 patients after the exclusion of other diseases that can also lead to gastrointestinal eosinophil infiltration. A positive correlation was observed between the duration of the symptoms and the risk of EGE (r = 0.18, P < 0.01). The patients whose symptoms persisted longer than 6 mo more readily developed EGE. None of the patients were considered to have EGE by their physicians before endoscopy. CONCLUSION: Although EGE is a rare inflammatory disorder, it is easily misdiagnosed. When a long history of abdominal symptoms fails to improve after conventional therapy, EGE should be considered.

Successful treatment of ileal ulcers caused by immunosuppressants in two organ transplant recipients.

Although gastroduodenal ulcers are common in solid organ transplant patients, there are few reports on multiple giant ulcers in the distal ileum and ileocecal valve caused by immunosuppressants Herein, we report on a liver transplant recipient and a renal transplant recipient with multiple large ulcers in the distal ileum and ileocecal valve who rapidly achieved ulcer healing upon withdrawal of sirolimus or tacrolimus and administration of thalidomide. In case 1, a 56-year-old man with primary hepatocellular carcinoma had received a liver transplantation. Tacrolimus combined with sirolimus and prednisolone was used as the anti-rejection regimen. Colonoscopy was performed because of severe abdominal pain and diarrhea at post-operative month 10. Multiple giant ulcers were found at the ileocecal valve and distal ileum. The ulcers healed rapidly with withdrawal of sirolimus and treatment with thalidomide. There was no recurrence during 2 years of follow-up. In case 2, a 34-year-old man with end-stage kidney disease received kidney transplantation and was put on tacrolimus combined with mycophenolate mofetil and prednisolone as the anti-rejection regimen. Twelve weeks after the operation, the patient presented with hematochezia and severe anemia. Colonoscopy revealed multiple large ulcers in the ileocecal valve and distal ileum, with massive accumulation of fresh blood. The bleeding ceased after treatment with intravenous somatostatin and oral thalidomide. Tacrolimus was withdrawn at the same time. Colonoscopy at week 4 of follow-up revealed remarkable healing of the ulcers, and there was no recurrence of bleeding during 1 year of follow-up. No lymphoma, tuberculosis, or infection of cytomegalovirus, Epstein-Barr virus, or fungus was found in either patient. In post-transplantation cases with ulcers in the distal ileum and ileocecal valve, sirolimus or tacrolimus should be considered a possible risk factor, and withdrawing them or switching to another immunosuppressant might be effective to treat these ulcers.

[Shikonin down-regulates CXCR4 expression and inhibits CXCL12-induced migratory responses in colorectal carcinoma cell line SW480].

OBJECTIVE: To investigate the effects of shikonin on the proliferation, expression of CXCR4 and the migratory responses to CXCL12 in colorectal carcinoma cell line SW480. METHODS: The proliferation of SW480 cells was assessed by MTT assay. Cell surface expression of CXCR4 was determined by flow cytometry. The migratory ability was determined by Transwell. RESULTS: Shikonin inhibited the proliferation of SW480 cells in time- and concentration-dependent manner. The expression rate of CXCR4 in SW480 cells was 99.1%. After application of shikonin 0.01 micromol/L, 0.1 micromol/L and 1.0 micromol/L for 24 h, the expression rate of CXCR4 decreased to 76.0%, 59.1% and 35.5% respectively (F=1098.041, P <0.001), and the CXCL12-induced SW480 cell migratory inhibition rate was 25.2%, 38.5% and 55.7% respectively (F=48.970, P <0.001). CONCLUSION: Besides having inhibiting tumor cell proliferation effect, Shikonin may also play a role in anti-metastasis via down-regulating the expression of CXCR4 and reducing the CXCL12-induced migratory response in colorectal carcinoma cell.

Activation of peroxisome proliferator-activated receptor-gamma induces apoptosis on acute promyelocytic leukemia cells via downregulation of XIAP.

In the present study we investigated the in vitro apoptosis inducing effects of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) ligand ciglitazone (CGZ) on acute promyelocytic leukemia (APL) NB4 cells and its mechanisms of action. The results revealed that CGZ (10-50 micromol/l) inhibited the growth of leukemia NB4 cells and caused apoptosis in a time- and dose-dependent manner. Apoptosis was observed clearly by flow cytometry (FCM) and DNA fragmentation analysis. After treatment by CGZ for 48 h, the percentage of disruption of mitochondrial membrane potential (Deltapsim) was increased in a dose-dependent manner. Western blotting demonstrated the cleavage of caspase-3 zymogen protein and a time-dependent cleavage of poly (ADP-ribose) polymerase (PARP). The results also demonstrated that PPAR-gamma expression was increased concomitantly when apoptosis occurred, and that CGZ-induced apoptosis was inhibited by the PPAR-gamma antagonist GW9662, suggesting a PPAR-gamma dependent signaling pathway in CZG-induced cell death. Moreover, CGZ treatment remarkably downregulated the expression of the X-linked inhibitor of apoptosis protein (XIAP), which was inhibited by GW9662. Of note, a small-molecule XIAP antagonist (1396-12) mimicked the effect of CGZ-induced apoptosis via activation of caspase-3, 7 and 9. The apoptosis-inducing effects by CGZ on fresh APL cells were also found to be remarkable by using FCM and Wright's staining observation. Taken together, our results suggest that downregulation of XIAP and activation of capase-3 play an important role in mediating the PPAR-gamma-dependent cell death induced by CGZ in APL cells. These data provide a novel insight into potential therapeutic strategies for treatment of leukemia.

The significance of Toll-like receptor 4 (TLR4) expression in patients with chronic hepatitis B.

PURPOSE: To investigate the importance of Toll-like receptor 4 (TLR4) expression on hepatocytes obtained from Chronic Hepatitis B patients as well as on hepatocellular carcinoma HepG2 and HepG2.2.15 cell lines. METHODS: Expression of TLR4 in liver tissues was determined by immunohistochemistry in 75 patients with CHB and in10 healthy controls. The protein and mRNA 1eve1s of TLR4 in hepatocellular carcinoma HepG2 and HepG2.2.15 cells were measured by flow cytometry (FCM) and real-time quantitative PCR (RQ-PCR), and endotoxin triggered TNF-alpha secretion in HepG2 and HepG2.2.15 cells was evaluated by ELISA. RESULTS: TLR4 expressed mainly in the cytoplasm and some on cell membrane in hepatocytes. The staining scores of TLR4 expression in the liver tissues of patients with CHB were significantly higher than that of healthy controls. The liver tissues from patients with severe CHB expressed higher level of TLR4 than those from patients with mild CHB. Furthermore, the staining scores of TLR4 expression in the liver tissues of patients with CHB were positively correlated with the grading scores. Our results also showed that the mean fluorescence intensity and TNF-alpha secretion induced by endotoxin as well as the protein and mRNA 1eve1s of TLR4 in HepG2.2.15 cells were all significantly higher than those in HepG2 cells. CONCLUSION: TLR4 was up-regulated in the hepatocytes in patients with CHB. This indicates a potentially important interaction between TLR4 expression and the pathogenesis of CHB.

[Expression of APRIL in colorectal carcinoma tissues and effects of chemotherapeutic agents on APRIL expression in colorectal carcinoma SW480 cells].

BACKGROUND & OBJECTIVE: A proliferation-inducing ligand (APRIL), a new member of the tumor necrosis factor (TNF) family, can stimulate tumor cell growth and proliferation both in vitro and in vivo. This research was to detect the expression of APRIL in colorectal carcinoma tissues, and to compare the effects of 5-fluorouracil (5-FU) and cisplatin (DDP) on the expression of APRIL in colorectal carcinoma SW480 cells. METHODS: The protein and mRNA levels of APRIL in 56 specimens of human colorectal carcinoma and para-tumor tissues and in SW480 cells were determined by immunohistochemistry and real-time fluorescence quantitative reverse transcription-polymerase chain reaction (FQ-RT-PCR). SW480 cells were treated with 5-FU and DDP at various concentrations for 24 h, 48 h and 72 h. The changes of APRIL mRNA level were analyzed by FQ-RT-PCR. RESULTS: Both positive rate and mRNA level of APRIL were significantly higher in colorectal carcinoma tissues than in para-tumor tissues (76.8% vs. 16.1%, 0.16+/-0.05 vs. 0.71+/-0.08, both P<0.001). The expression of APRIL was strong in SW480 cells. When treated with different concentrations of 5-FU, the mRNA level of APRIL in SW480 cells raised gradually and reached the highest levels at 72 h after treatment (0.85+/-0.10, 0.81+/-0.09, 0.83+/-0.11, and 0.90+/-0.12 at the concentrations of 25, 50, 100 and 200 microg/mL, respectively), which were significantly higher than those in blank control group (P<0.001). When treated with different concentrations of DDP, the mRNA level of APRIL in SW480 cells did not increase when compared with that in control group (P>0.05). After 72-hour treatment, the mRNA level of APRIL in SW480 cells was significantly lower in 10 microg/mL and 20 microg/mL DDP groups than in blank control group (0.44+/-0.05 and 0.40+/-0.07 vs. 0.57+/-0.06, P<0.05). CONCLUSIONS: APRIL may promote the development of colorectal carcinoma. When chemotherapy is conducted to treat colorectal carcinoma, especially when 5-FU is included in the regimen, anti-APRIL therapy might be an important assistant treatment to counter the impact of APRIL caused by antitumor drugs.

[A close relationship between viral hepatitis B and Toll-like receptor 2].

OBJECTIVE: To investigate the relationship of Toll-like receptor 2 (TLR2) and viral hepatitis B through testing the expression of TLR2 in liver tissues of patients infected with HBV and in HepG2 and HepG2.2.15 cell lines. METHODS: Expression of TLR2 was determined by Elivision immunohistochemistry in liver tissues from patients with chronic viral hepatitis B (CHB), chronic severe hepatitis (CSH), from healthy controls and from cells of HepG2 and HepG2.2.15 hepatocellular carcinoma cell lines. Direct immunofluorescence flow cytometry was used to detect TLR2+ cell percentage and mean fluorescence intensity (MFI). RESULTS: The intensity of TLR2 expression in liver tissues of CHB and CSH was significantly higher than that of the healthy controls (probability value less than 0.01). The positive staining was mainly located in the cytoplasm and on some cell membranes. In CHB, the intensity of TLR2 expression was positively correlated with the grade of necroinflammatory activity (r=0.597, P less than 0.01). There were significant differences of serum total bilirubin levels with different grades of positive staining of TLR2 (P less than 0.05). In liver tissues of the CHB patients, the positive staining of TLR2 was shown in small foci. MFI of TLR2 (10.7+/-2.8) and TLR2+ cell percentage (16.3%+/-7.0%) of HepG2.2.15 cells were both significantly higher than those of HepG2 cells (1.0+/-0.3, 0.4%+/-0.1%, P less than 0.01). CONCLUSIONS: Expression of TLR2 is closely correlated with hepatitis B, especially to the grades of its necroinflammatory activity.