By performing broad range PCR, we verified that the first 19 exons of FGFR2 were present at the 5′end and included an intact open reading frame and kinase domains. Whole-genome sequencing of the tumor and matched normal tissue verified the presence of an inverted translocation between the two chromosomes in the tumor but not in the normal tissue. 108 cases of ICC were analyzed by RT-PCR and Sanger sequencing for the presence of the same fusion event. The screening revealed that 21 out of 108 ICCs (19. 4%) harbored the same alteration. To verify if PPHLN1 is able to mediate dimerization of the receptor, we expressed hystidine-tagged

fusion gene in NIH3T3 cells and verified its oligomerization, suggesting PD-0332991 solubility dmso constitutive activation. NIH3T3 over-expressing the fusion gene showed enhanced migration capability (p<0. 02). CONCLUSIONS: A novel fusion event including an active tyrosine kinase was discovered in 20% of ICC cases by next-generation sequencing. The identified fusion gene is caused by a DNA rearrangement and increases cell migration capability in vitro. This novel fusion may represent an appealing target for selected molecular therapies. Disclosures: Myron Schwartz - Consulting: Gilead, Inova Vincenzo Mazzaferro - Advisory Committees or Review Panels: Bayer; Grant/Research Support: Nordion; Speaking and Teaching: Merck

Serono S. p. A. Eric Schadt – Advisory Committees or Review Panels: Pacifici Biosciences, Numedii, GNS MCE Selleck MLN8237 Healthcare, Ingenuity, Whole Biome; Board Membership: Sage Bionetworks Josep M. Llovet – Consulting: Bayer Pharmaceutical, Bristol Myers Squibb, Imclone, Biocompatibles, Novartis; Grant/Research Support: Bayer Pharmaceutical,

Bristol Myers Squibb, Boehringer-Ingelheim The following people have nothing to disclose: Daniela Sia, Bojan Losic, Kate Revill, Ke Hao, Laia Cabellos, Zhongyang Zhang, Yujin Hoshida, Sasan Roayaie, Swan N. Thung, Samuel Waxman Cholangiocarcinoma (CCA) is a cancer of the biliary tree arising from inflammation and injury, and aberrant expression of microRNAs has been implicated in CCA; miR-106b is a candidate oncoMir in CCA. Purpose: Expression of miR-106b is increased in CCA but the specific pathways affected and genes involved remain to be elucidated. We hypothesized that miR106b regulates apoptosis and proliferation in CCA by targeting key regulatory proteins. Methods: Cholangiocyte cell lines were employed: non-malignant, H69; and malignant, KMCH, Mz-ChA-1, and HuCCT. RNA isolation was performed by silica membrane binding and quality checked by microcapillary electrophoresis. Apoptosis was measured by nuclear morphology. miR-106b expression was increased or decreased by transfection of mature miR-106b or locked nucleic acid (LNA) antagonist, respectively. Results: Unbiased, next-generation RNA sequencing revealed 129 targets exhibiting statistically significant differential expression between miR-106b and LNA treatments.

5 It offers a standardized way of preparing reports of trial findings that facilitates accurate and transparent reporting with critical appraisal and interpretation. More and more highly cited academic journals, including HEPATOLOGY, have adopted the CONSORT statement for standardization and integrity. In China, CONSORT for TCM has been

developed and widely adopted; it provides more specificity and sensitivity for the assessment of TCM methodological quality.6 Therefore, it would have been much better if the CONSORT standard, instead of selleck chemicals Jadad scoring, had been used in this meta-analysis. In summary, the methodological quality of the analysis needs to be reassessed. Ming-Hua Zheng M.D.*, Yu-Chen Fan M.D.†, Ke-Qing Shi M.D.*, Yong-Ping Chen M.D.*, * Liver Research Center, Department of Infection and Liver Diseases, First

Affiliated Hospital, Wenzhou Medical College, Wenzhou, China, † Department of Hepatology, Qilu Hospital, Shandong University, Jinan, China. “
“We read the article by Horiguchi et VX-770 cost al.1 with great interest. It is a commonly accepted dogma that inflammation induces necrosis and apoptosis of hepatocytes during liver damage. However, clinicians have found that inflammation does not always correlate with hepatocellular damage in chronic liver disease. How to explain the conflict? By using a well-established model of mice with specific deletion of signal transducer and activator of transcription 3 in myeloid cells (STAT3mye−/−), Horiguchi and colleagues surprisingly found more inflammatory cells, eg, neutrophils, but less necrosis/apoptosis in the liver of STAT3mye−/− mice than in wild-type mice after carbon tetrachloride (CCl4) treatment. STAT3mye−/− mice had higher hepatic STAT3 activation and became resistant to hepatic oxidative stress after CCl4 injection compared with wild-type

mice. In contrast to STAT3mye−/− mice, hepatocyte-specific STAT3 knockout (STAT3Hep−/−) mice had more liver necrosis/apoptosis but less inflammation after CCl4 treatment compared with wild-type mice. An additional 上海皓元 deletion of hepatocyte STAT3 in STAT3mye−/− mice restored CCl4-induced hepatic necrosis but reduced liver inflammation. This study suggests that inflammation associated with a predominance of hepatoprotective cytokines may reduce rather than accelerate hepatocellular damage via activation of hepatocyte STAT3 in CCl4-induced liver damage. The data elucidate a potential mechanism that inflammation does not always correlate with hepatocellular damage. Interestingly, the same group had also previously investigated inflammation and hepatocellular damage in the same strain of STAT3mye−/− mice treated with concanavalin A (ConA) or ethanol.

The 5-year survival rate for untreated, symptomatic HCC is < 5%. In contrast, the 5- year survival rate in patients with cirrhosis following transplantation of small (2 cm) HCC is 80%. The detection of small HCC is clearly critical to patient outcome. Although many CT and magnetic resonance (MR)

imaging studies have reported high diagnostic accuracy for HCC and Dysplastic Nodules (DN) in patients with cirrhosis, most of these have been limited by study Selleckchem Aloxistatin design, incomplete pathologic correlation and suboptimal imaging techniques. Correlation between explant pathology and pretransplant radiology is of prime importance- among other factors- to choose the suitable line of treatment for liver nodules in cirrhotic patients including follow up, locoregional therapy, liver transplantation or paliative treatment. Methods: 100 patients who underwent liver transplantation at our institution between 2002 and 2013 for the presence of HCC were retrospectively reviewed. Liver transplantation was performed Copanlisib either as primary treatment or following bridging locoregional treatment. HCC was radiologically diagnosed. Radiological diagnosis was performed using one or two contrast enhanced dynamic imaging studies

including Multidetector computed tomography (MDCT) and MRI. Pathological examination was made using whole liver explant examination by senior pathologists who have experience in liver pathology. Pathologists had knowledge about the pretransplant radiological findings. Radiological and pathological correlation

was made between explant pathology and radiological findings. Correlation was made on per nodule level including size, location and nature. Results: A total 230 nodules were identified in explant pathology from 100 liver transplant patients. Overall; 208 nodules were radiologically identified before transplant (90.4%), while pretransplant imaging modalities failed to show 22 nodules (9.6%). Out of the missed nodules 10 HCC lesions and 12 dysplastic nodules (4.3% and 5.2 % out of all lesions respectively) were pathologically identified. Out of the identified nodules 59 were misinterpreted.114 nodules were found to be more than or MCE公司 equal to 2cm in maximum dimensions by pathology (group 1)compared to 67 between 1and 2 cm (group2) and 49 less than 1 cm (group 3). percentage of the missed or misinterpreted nodules was significantly less in first group as compared to the other two group, (p=0.000) Conclusion: pretransplant imaging modalities are very relaible in diagnosis of cirrhotic liver nodules specially in smalll lesions Disclosures: Hussien Elsiesy – Speaking and Teaching: ROCHE, BMS, JSK The following people have nothing to disclose: Mohamed R. Abdelfattah, Hadeel Al-mana, Mohamed Neimatallah, Mohammed Al-sebayel, Dieter C.

[65-70] Thus, the concept of “gastric cytoprotection” is not only still relevant, and the underlying mechanisms still need to be investigated, but the future for the introduction of new drugs which protect the stomach without interfering with its physiologic functions (e.g. acid secretion) is very promising. It is hence not surprising that although some conferences on this topic have been discontinued, another series of international symposia devoted to cell injury and cytoprotection are still continuing.[71] Our original studies

performed at the Brigham and Women’s Hospital/Harvard Medical School (in Boston, MA) were supported by RO1 grants and RCDA from NIH, while the experiments performed at the VA Medical Center/University of California, Irvine, School of Medicine see more (in Long Beach/Irvine) were made possible mainly by VA Merit Review grants. I also want to the thank Dr XM Deng for his assistance GSK2126458 mouse with the preparing some of the figures and references. “
“This practice guideline has been approved by the American Association for the Study of Liver Diseases (AASLD) and endorsed by the Infectious Diseases Society of America, the American College of Gastroenterology and the

National Viral Hepatitis Roundtable. These recommendations provide a data-supported approach to establishing guidelines. They are based on the following: (1) 上海皓元医药股份有限公司 a formal review and analysis of the recently published world literature on the topic (MEDLINE search

up to June 2011); (2) the American College of Physicians’ Manual for Assessing Health Practices and Designing Practice Guidelines;1 (3) guideline policies, including the AASLD Policy on the Development and Use of Practice Guidelines and the American Gastroenterological Association’s Policy Statement on the Use of Medical Practice Guidelines;2 and (4) the experience of the authors in regard to hepatitis C. Intended for use by physicians, these recommendations suggest preferred approaches to the diagnostic, therapeutic, and preventive aspects of care. They are intended to be flexible, in contrast to standards of care, which are inflexible policies to be followed in every case. Specific recommendations are based on relevant published information. To more fully characterize the quality of evidence supporting recommendations, the Practice Guidelines Committee of the AASLD requires a Class (reflecting benefit versus risk) and Level (assessing strength or certainty) of Evidence to be assigned and reported with each recommendation (Table 1, adapted from the American College of Cardiology and the American Heart Association Practice Guidelines).

In a Japanese study that considered 50 years as the cut-off age, frequency of FD was found to be lower among persons older than 50 years.29 In another study from Japan, of 1730 gastric cancer patients, 27 were less than 34 years old.30 A study from India showed that patients with gastric cancer were older than patients with non-ulcer dyspepsia (53 ± 12 years vs 43 ± 13 years).31 These data might suggest that the

cut-off age for considering endoscopic examination may vary by geographical area, though most believe that it should be 45 years of age. Statement 9. A portion of Asian patients with functional dyspepsia has overlapping irritable bowel syndrome. Grade of evidence: moderate. Level of agreement:

a: 100.0%; b: 0%; c: 0%; d: 0%; e: 0%; f: 0%. In Asian patients, there is a significant find more overlap between FD and IBS. In a Chinese study using the Rome III criteria, 24.8% of FD patients had overlapping IBS.8 In a study from India, dyspepsia-IBS overlap (dyspepsia was defined as abdominal pain or discomfort centered in the upper abdomen and IBS by Manning’s criteria) was found in 14.2% of the FD subjects.32 Another Indian multi-center study demonstrated a high frequency (90%) of upper abdominal pain or discomfort in IBS patients, although the diagnosis in that study was based on the clinicians’ assessment rather than on the Rome criteria.33 In a Japanese study, the overlap of FD and IBS was found to be 3.5%

of the patients with FD.34 In a study from Hong Kong learn more using the Rome I criteria, overlapping IBS was found to be 16.9% of the subjects with dyspepsia.35 In a Japanese study using the Rome II criteria for the diagnosis MCE of functional GI disorders, 181 medical students were recruited, and the overlap of IBS was found to be 66.7% of UD subjects.36 In a Korean study of 476 patients with functional GI disorders according to the Rome II criteria, the overlap of IBS was found in 20.8% of FD patients.26 In these studies, overlap of FD and IBS showed wide variation that might be due to diagnostic criteria, study populations, sociocultural issues, or symptom reporting by the patients. Statement 10. Patients with functional dyspepsia may have overlap with gastroesophageal reflux disease. Grade of evidence: moderate. Level of agreement: a: 84.2%; b: 15.8%; c: 0%; d: 0%; e: 0%; f: 0%. Overlap of FD and gastroesophageal reflux disease (GERD) is common in different Asian populations.23 A study from Turkey showed overlap of GERD to be 29.4% of subjects with symptoms of dyspepsia,37 and a study from Korea showed such overlap to be 24.1% of FD subjects.38 In both of those studies, GERD was diagnosed by questionnaire and not by 24-h pH-impedance monitoring, which is currently the gold standard for diagnosis of GERD.

His successful academic career started at Harvard Medical School in 1961 and proceeded until becoming Professor of Medicine at Northwestern University Medical School, Chicago, IL. After retirement in 1995, he spent 3 years in Amsterdam, NL to then move to Seattle to be appointed Affiliated Professor of Medicine at the University of Washington

where he was actively involved in research and preparing teaching material for a highly appreciated GE course. Dr. Ostrow served as president of the American Association for the Study of Liver Diseases in 1986-1987. Don Ostrow has been and will remain a giant in the field of bilirubin and jaundice. He was among the few persons who understood back in the 1960s the importance selleck kinase inhibitor Erlotinib solubility dmso and the pivotal role of the yellow pigment until then considered only as a waste product. Due to his unmatched scientific curiosity, Don realized that bilirubin might have important biological functions crucial to several metabolic pathways. Almost all of these theories have been proven correct as more advanced experimental techniques became available. Taking advantage of his scientific background in both chemistry and medicine, Don combined this dual physical chemical and clinical approach to the study of bilirubin. His unique discoveries made Don one of the first real translational researchers

in hepatology. The determination of the solubility of bilirubin in aqueous media, the binding constants to albumin, and their role in the metabolic and toxic effects of the pigment shed totally new light on bilirubin neurotoxicity in the newborn and paved the

way to more sophisticated investigations aimed at understanding the molecular events associated with the neurotoxicity and therefore its prevention. His contributions to the chemical and biological characteristics of bilirubin will remain landmarks for anyone involved in the study of the pigment, either in the experimental or clinical arena. The translational approach in medicine, rather new back in 1960s and 1970s, made his laboratory the place to be for young fellows to be trained and share front-row studies of the correlation between the chemical structure and the biological behavior of bilirubin and bile acids. Anyone who had MCE the privilege to work with Don admired his analytic mind, his ability to interpret experimental data, to criticize experimental flaws, and to put new observations in perspective. This was particularly true when Don discussed science with young investigators—a tough mentor who could issue sharp critiques but at the same time precious suggestions and encouragement to continue what she/he was doing. The ability to grasp the critical points after a complicated presentation of sophisticated molecular biology data was remarkable.

Post EUS/FNA diagnosis showed pseudocyst (46.8%), serous cystadenoma (16.2%), intraductal papillary neoplasm (9%), mucinous cystadenoma (12.6%), neuroendocrine tumour (3.6%), solid pseudopapillary tumour (0.9%) and cystic ductal adenocarcinoma (8.1%). EUS/FNA changed the diagnosis and management in 33.3% (37/111) of the patients. Seventeen patients (45.9%) who were initially diagnosed with benign cyst on imaging had diagnosis changed to malignant/ premalignant

cysts. Only 10 patients underwent surgical resection, 9/10 had malignancy on resection histology. Of the 7 who did not undergo surgery, 4 had metastasis, 2 had premalignant cyst and 1 declined surgery. Twenty (54%) patients who were initially diagnosed with a malignant lesion did not require surgery after EUS/FNA changed the diagnosis. Of these 20, none develop malignant lesion after 6 months of surveillance. The sensitivity and specificity of EUS/FNA and imaging to Selleck AP24534 accurately determine the nature of pancreatic cyst are 75% and 81.1% vs. 25% and 68.4% respectively (P value <0.05). Conclusion: EUS/FNA has valuable role in the management of pancreatic cyst. It is more accurate than imaging alone and can correctly stratify which patients should undergo resection. Key Word(s): 1. Pancreatic cyst; 2. EUS; 3. Imaging; Presenting Author: XIAOYONG WANG Additional Authors: LENING XUE Corresponding

Author: XIAOYONG WANG Affiliations: Changzhou No. 2 Hospital, Affiliated with Nanjing Medical University Objective: Recently, several studies have evaluated the association between hepatitis B virus Talazoparib (HBV) infection and pancreatic cancer risk; however, results have been inconsistent. The goal of this study was to perform a meta-analysis of the published data to evaluate this association. Methods: A search of relevant studies published up to May 2012 was performed. After reviewing each study, extracting data, and evaluating heterogeneity and publication bias, a meta-analysis was performed to evaluate the association of HBV infection and pancreatic cancer risk.

Subgroup analyses were carried out according to the original studies’ designs and separate meta-analyses were performed. Pooled odds ratios (ORs) with 95% confidence intervals MCE (CIs) were calculated using the fixed- or random-effect models. Results: Nine studies, encompassing seven case-control and two cohort studies, were analyzed. Overall, there was an association between hepatitis B surface antigen (HBsAg) -positive carrier state and a higher risk of pancreatic cancer (OR = 1.24, 95% CI: 1.08 to 1.43). Among the case-control studies, the HBsAg carrier state (HBsAg-positive: OR = 1.24, 95% CI: 1.06 to 1.46) and past exposure to HBV without evidence of HBV recovery (HBsAg-negative/anti-HBc-positive/anti-HBs-negative: OR = 1.76, 95% CI: 1.29 to 2.39) were significantly associated with pancreatic cancer risk.

Post EUS/FNA diagnosis showed pseudocyst (46.8%), serous cystadenoma (16.2%), intraductal papillary neoplasm (9%), mucinous cystadenoma (12.6%), neuroendocrine tumour (3.6%), solid pseudopapillary tumour (0.9%) and cystic ductal adenocarcinoma (8.1%). EUS/FNA changed the diagnosis and management in 33.3% (37/111) of the patients. Seventeen patients (45.9%) who were initially diagnosed with benign cyst on imaging had diagnosis changed to malignant/ premalignant

cysts. Only 10 patients underwent surgical resection, 9/10 had malignancy on resection histology. Of the 7 who did not undergo surgery, 4 had metastasis, 2 had premalignant cyst and 1 declined surgery. Twenty (54%) patients who were initially diagnosed with a malignant lesion did not require surgery after EUS/FNA changed the diagnosis. Of these 20, none develop malignant lesion after 6 months of surveillance. The sensitivity and specificity of EUS/FNA and imaging to CT99021 mw accurately determine the nature of pancreatic cyst are 75% and 81.1% vs. 25% and 68.4% respectively (P value <0.05). Conclusion: EUS/FNA has valuable role in the management of pancreatic cyst. It is more accurate than imaging alone and can correctly stratify which patients should undergo resection. Key Word(s): 1. Pancreatic cyst; 2. EUS; 3. Imaging; Presenting Author: XIAOYONG WANG Additional Authors: LENING XUE Corresponding

Author: XIAOYONG WANG Affiliations: Changzhou No. 2 Hospital, Affiliated with Nanjing Medical University Objective: Recently, several studies have evaluated the association between hepatitis B virus Rucaparib chemical structure (HBV) infection and pancreatic cancer risk; however, results have been inconsistent. The goal of this study was to perform a meta-analysis of the published data to evaluate this association. Methods: A search of relevant studies published up to May 2012 was performed. After reviewing each study, extracting data, and evaluating heterogeneity and publication bias, a meta-analysis was performed to evaluate the association of HBV infection and pancreatic cancer risk.

Subgroup analyses were carried out according to the original studies’ designs and separate meta-analyses were performed. Pooled odds ratios (ORs) with 95% confidence intervals 上海皓元医药股份有限公司 (CIs) were calculated using the fixed- or random-effect models. Results: Nine studies, encompassing seven case-control and two cohort studies, were analyzed. Overall, there was an association between hepatitis B surface antigen (HBsAg) -positive carrier state and a higher risk of pancreatic cancer (OR = 1.24, 95% CI: 1.08 to 1.43). Among the case-control studies, the HBsAg carrier state (HBsAg-positive: OR = 1.24, 95% CI: 1.06 to 1.46) and past exposure to HBV without evidence of HBV recovery (HBsAg-negative/anti-HBc-positive/anti-HBs-negative: OR = 1.76, 95% CI: 1.29 to 2.39) were significantly associated with pancreatic cancer risk.

Post EUS/FNA diagnosis showed pseudocyst (46.8%), serous cystadenoma (16.2%), intraductal papillary neoplasm (9%), mucinous cystadenoma (12.6%), neuroendocrine tumour (3.6%), solid pseudopapillary tumour (0.9%) and cystic ductal adenocarcinoma (8.1%). EUS/FNA changed the diagnosis and management in 33.3% (37/111) of the patients. Seventeen patients (45.9%) who were initially diagnosed with benign cyst on imaging had diagnosis changed to malignant/ premalignant

cysts. Only 10 patients underwent surgical resection, 9/10 had malignancy on resection histology. Of the 7 who did not undergo surgery, 4 had metastasis, 2 had premalignant cyst and 1 declined surgery. Twenty (54%) patients who were initially diagnosed with a malignant lesion did not require surgery after EUS/FNA changed the diagnosis. Of these 20, none develop malignant lesion after 6 months of surveillance. The sensitivity and specificity of EUS/FNA and imaging to Cell Cycle inhibitor accurately determine the nature of pancreatic cyst are 75% and 81.1% vs. 25% and 68.4% respectively (P value <0.05). Conclusion: EUS/FNA has valuable role in the management of pancreatic cyst. It is more accurate than imaging alone and can correctly stratify which patients should undergo resection. Key Word(s): 1. Pancreatic cyst; 2. EUS; 3. Imaging; Presenting Author: XIAOYONG WANG Additional Authors: LENING XUE Corresponding

Author: XIAOYONG WANG Affiliations: Changzhou No. 2 Hospital, Affiliated with Nanjing Medical University Objective: Recently, several studies have evaluated the association between hepatitis B virus BTK signaling pathway inhibitors (HBV) infection and pancreatic cancer risk; however, results have been inconsistent. The goal of this study was to perform a meta-analysis of the published data to evaluate this association. Methods: A search of relevant studies published up to May 2012 was performed. After reviewing each study, extracting data, and evaluating heterogeneity and publication bias, a meta-analysis was performed to evaluate the association of HBV infection and pancreatic cancer risk.

Subgroup analyses were carried out according to the original studies’ designs and separate meta-analyses were performed. Pooled odds ratios (ORs) with 95% confidence intervals 上海皓元医药股份有限公司 (CIs) were calculated using the fixed- or random-effect models. Results: Nine studies, encompassing seven case-control and two cohort studies, were analyzed. Overall, there was an association between hepatitis B surface antigen (HBsAg) -positive carrier state and a higher risk of pancreatic cancer (OR = 1.24, 95% CI: 1.08 to 1.43). Among the case-control studies, the HBsAg carrier state (HBsAg-positive: OR = 1.24, 95% CI: 1.06 to 1.46) and past exposure to HBV without evidence of HBV recovery (HBsAg-negative/anti-HBc-positive/anti-HBs-negative: OR = 1.76, 95% CI: 1.29 to 2.39) were significantly associated with pancreatic cancer risk.

23 The present study suggests a novel role for the CCR9/CCL25 axis in the process leading to persistent liver injury and subsequent liver fibrosis, as summarized in Fig. 7C. Deficiency in CCR9 protected the liver from overt fibrosis in two different murine models,

as well as causing decreased infiltration of macrophages into the liver. The crucial role of recruited macrophages has been emphasized previously in several experimental models.3 Various chemokines are involved at different stages of inflammation and are highly tissue-specific.14, 29, 31 In murine models of liver fibrosis, the essential roles of CCR2-dependent monocytes have been reported, and are similar PD0325901 purchase to the monocytes recruited to livers with acute injury,9 while CCR5-dependent fibrogenesis is prominent in the later process of fibrosis.10 A possible role for the CCR9/CCL25 axis in the pathogenesis of experimental PF-02341066 order atherosclerosis, a chronic inflammatory state, was recently reported.32 CCR9+ macrophages in the synovial fluid may also play a role in the pathogenesis of rheumatoid arthritis, a chronic inflammatory disease.33 These findings suggest a possible immunological role for CCR9+ macrophages in chronic inflammation in various tissues. The present study is the first to demonstrate that CCR9+ macrophages affect chronic inflammation and subsequent

fibrosis in the liver. It is important to clarify the relevance of the CCR9/CCL25 axis during the

development of liver fibrosis in our model. First, we carefully evaluated the source of CCR9-positive cells by isolating each cell fraction in fibrotic livers and found that CCR9 expression was up-regulated only in macrophages and HSCs, together with the up-regulation MCE of CCL25 in LSECs. Regarding the cellular location of CCR9, dual-color immunofluorescence analysis demonstrated the colocalization of CCR9 on macrophages and HSCs around periportal areas where profound matrix deposition occurs in various liver fibrosis models. Several observations support our hypothesis that CCR9+ macrophages are key factors in processing wound healing and subsequent liver fibrosis. First, numbers of CCR9+CD11b+ macrophages with an activated phenotype and high TNF-α production dramatically increased in experimental fibrotic livers. Second, CCR9 deficiency resulted in reduced infiltration of CD11b+ macrophages to the liver and subsequent attenuation of fibrosis. Third, and most important, in vitro coculture analysis revealed that CD11b+ macrophages from CCl4-treated WT mice (i.e., the existence of CCR9+ macrophages), but not CD11b+ macrophages from CCl4-treated CCR9−/− mice (CCR9− macrophages) have the potential to activate HSCs by up-regulating α-SMA, TGF-β1, collagen 1α1, and TIMP-1 mRNA. Molecular interactions between macrophages and HSCs are important for promoting fibrosis.