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ABSTRACT: OBJECTIVES: Clinically relevant postoperative pancreatic fistula (POPF) after pancreatoduodenectomy is often accompanied by bacterial infection. To elucidate the mechanism of bacterial infection associated with POPF, we investigated the relationship between POPF and bacteria isolated from ascitic fluid and removed drains. METHODS: Subjects were 101 patients who had undergone pancreatoduodenectomy. Microbial culture was performed using ascitic fluid obtained from drains. We also compared the isolated bacteria from removed drains on postoperative day (POD) 4 and after POD 7. RESULTS: In 23 patients (22.8%), microbial cultures were already positive on POD 1, although purulent discharge was not observed. Among patients with grade B/C POPF, bacteria were detected on POD 1 in 53.8%; these isolated bacteria were the same as those isolated after POPF formation. In contrast, only 7.7% of patients with grade A POPF were positive on POD 1. The number of bacteria isolated from drains removed after POD 7 significantly increased compared with those isolated from drains removed on POD 4. CONCLUSIONS: Bacterial contamination in ascitic fluid may be an initiating event that leads to the development of clinically relevant POPF. Therefore, it is important to perform both the administration of the appropriate antibiotics and early drain removal.
Pancreas 02/2013; · 2.39 Impact Factor
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ABSTRACT: Type IV-A choledochal cysts (CCs) are a congenital biliary anomaly which involve dilatation of the extrahepatic and intrahepatic bile ducts. We present the case of a 30-year-old woman with type IV-A CC, on whom three-dimensional computed tomography (3D CT) and virtual endoscopy were performed. 3D CT revealed partial dilatation in the posterior branch of the intrahepatic bile duct and a relative stricture between it and the extrahepatic bile duct. Virtual endoscopy showed that this stricture was membrane-like and separated from the surrounding blood vessels. Based on these image findings, complete cyst resection, bile duct plasty for the stricture, and hepaticojejunostomy were safely performed. To the best of our knowledge, there are no reports of imaging by virtual endoscopy of the biliary tract which show the surrounding blood vessels running along the bile duct.
World Journal of Gastroenterology 07/2012; 18(28):3761-4. · 2.47 Impact Factor
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ABSTRACT: We previously reported that the administration of bevacizumab for pancreatic neuroendocrine tumors inhibited angiogenesis in the host, resulting in tumor growth inhibition. In light of these results, we compared the effect of bevacizumab/gemcitabine/S-1 combination therapy vs. bevacizumab monotherapy. The QGP-1 pancreatic neuroendocrine carcinoma cell line and the BxPC-3 ductal cell carcinoma cell line were transplanted into the subcutaneous tissue of mice, and the mice were treated for 3 weeks with bevacizumab [50 mg/kg intraperitoneally (i.p.) twice weekly], gemcitabine (240 mg/kg i.p. once weekly) and S-1 (10 mg/kg orally five times weekly). The antitumor effect and side effects were evaluated by measuring the tumor volume and weight and by changes in body weight, respectively. The tumor volume became smaller (from the maximum volume) in the group treated with bevacizumab, gemcitabine and S-1 (BGS) and the group treated with bevacizumab and gemcitabine (BG). A significant difference was noted in the tumor weight between the BG group and the group treated with bevacizumab alone. A relatively significant decrease in the body weight was observed in the BGS and BG groups. We conclude that gemcitabine is appropriate as a drug used in combination with bevacizumab for pancreatic neuroendocrine tumors.
Experimental and therapeutic medicine 04/2012; 3(4):599-602.
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ABSTRACT: Since there is a difference in the slice thickness between preoperative images of liver metastases (1-3mm slices) and surgical liver pathology specimens (5mm slices), micrometastases may not be detected in these specimens. In addition, the accuracy of preoperative imaging for the detection of metastases degenerated by chemotherapy is unclear.
Five patients with liver metastases from colorectal cancer who had received adjuvant chemotherapy and undergone hepatectomy were included. The whole resected liver was sliced at approximately 1mm intervals and the slices were examined carefully for gross lesions. The preoperative CT and EOB-MRI findings of each lesion were compared with gross and histopathological findings.
The accuracy of EOB-MRI was higher than that of CT for the detection of liver metastases. The number of lesions detected on EOB-MRI was in agreement with that of histopathologically proven liver metastases in 4 of the 5 patients. All lesions that were grossly identified but turned out to be non-neoplastic were regenerative nodules associated with drug-induced liver injury or lobular nodules associated with marked fatty change, measuring about 1mm in diameter.
EOB-MRI was the most accurate method for the preoperative detection of liver metastases, enabling the visualization of almost all liver metastases.
Hepato-gastroenterology 03/2012; 59(116):981-5. · 0.66 Impact Factor
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ABSTRACT: In addition to the use of chemotherapeutic agents for the prevention of multiple liver metastases from colorectal cancer, the anti-vascular endothelial growth factor (VEGF) antibody, bevacizumab, is often used, and its effectiveness has been established. By contrast, it has been reported that the use of bevacizumab prior to or following surgery delays wound healing or liver regeneration. In this study, we investigated whether the administration of bevacizumab following hepatectomy inhibits remnant liver regeneration or the growth of remnant metastases. Mice were partially hepatectomized (31% of the liver was removed), transplanted with the murine colorectal cancer cell line, CT26, in the remnant lobe, and intraperitoneally injected with bevacizumab (4 mg/kg) for a total of 6 times. Serum VEGF levels were measured on day 1 following surgery, and each lobe of the liver was weighed on day 14. Serum VEGF levels in non-hepatectomized, tumor-bearing mice exceeded those in their non-tumor-bearing counterparts; however, the administration of bevacizumab did not reduce the serum VEGF levels. The volume of the liver lobe of the hepatectomized, CT26-transplanted and non-CT26-transplanted mice was 1,349.6 and 735.5 mg, respectively, indicating rapid growth of the CT26 transplant (p=0.023). The volume of the CT26-transplanted lobe of the bevacizumab-administered mice was 1,379.0 mg, which was not significantly different from that (1,349.6 mg) of the non-bevacizumab-administered mice. The volume of the remnant lobe of the bevacizumab-administered mice was 1,051.0 mg, which did not significantly differ from that (957.3 mg) of the non-bevacizumab-administered mice. The administration of bevacizumab following hepatectomy did not delay remnant liver regeneration, and did not suppress the growth of metastases in the remnant lobes or remnant liver regeneration.
Experimental and therapeutic medicine 02/2012; 3(2):347-350.
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ABSTRACT: Single nucleotide polymorphism (SNP) of the genes for ATP-binding cassette transporters is related to the side effects of anticancer drugs and that of drug metabolism-related enzyme genes is involved in the activation of gemcitabine (GEM).
Forty eight patients treated with adjuvant GEM chemotherapy after pancreatic cancer resection was examined for the SNP of multidrug-resistance 1 (MDR1) 2677, MDR1 3435, breast cancer resistance protein (BCRP) 421, ribonucleotide reductase M1 (RRM1)(-)524, RRM1(-)37 and deoxycytidine deaminase (CDA) 208. We divided the patients according to normal group: patients homozygous for a wild-type allele or heterozygous for a mutant allele and mutant group: those homozygous for a mutant allele. Both groups were compared regarding the outcome and the occurrence and severity of side effects.
MDR1 2677, MDR1 3435, BCRP421, RRM1(-) 524, RRM1(-) 37 and CDA mutant groups comprised 37.5, 31.3, 0, 12.5, 4.2 and 4.2%, respectively. The occurrence of >G3 side effects was the most frequent in the MDR1 2677 mutant group at 39%. The disease-free survival and overall survival tended to be longer in the MDR1 2677 mutant group.
A correlation between the SNP of MDR1 2677 and drug response in patients receiving GEM chemotherapy.
Hepato-gastroenterology 12/2011; 59(117):1609-13. · 0.66 Impact Factor
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ABSTRACT: The normal pancreas has an abundant blood flow, in contrast to pancreatic cancer, which is a hypovascular tumor. During hypoxia under a hypovascular environment, the transcription factor hypoxia-inducible factor-1α (HIF-1α) is activated. High HIF-1α expression reduces sensitivity to gemcitabine (GEM) which is used as a treatment for pancreatic cancer. The objective of this study was to clarify HIF-1α expression in pancreatic cancer and the association of its effects to GEM treatment. We used the human pancreatic ductal carcinoma cell lines AsPC-1 and BxPC-3 to evaluate cell proliferation, HIF-1α protein expression and sensitivity to GEM in a hypoxic environment of 1% O2 in 48 pancreatic cancer patients who received adjuvant GEM treatment after pancreatectomy. We divided the patients according to HIF-1α expression and the presence of single nucleotide polymorphisms, and we based our evaluation on the adverse events associated with GEM chemotherapy and patient outcome. The hypoxic environment promoted cell proliferation, induced HIF-1α expression and increased GEM resistance, especially in AsPC-1 cells, which included a mutant homozygote for HIF-1α(C1772T). There were no significant differences between the HIF-1α(-) and HIF-1α(+) groups in either adverse events or patient outcomes. HIF-1α enhanced neo-microvascularity in a hypoxic environment and increased drug resistance. The period until recurrence was shorter in the patients with a strong HIF-1α expression, than that in those with a weak HIF-1α expression.
Oncology Reports 09/2011; 26(6):1399-406. · 1.84 Impact Factor
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ABSTRACT: Anticancer drugs are essential to pancreatic cancer therapy. The multidrug-resistance 1 (MDR1) gene codes for one of the ATP binding cassette (ABC) transporters. The neutralizing antibody of MDR1 reduces the activity of MDR1 and may add to the sensitivity of anti-cancer drugs. We investigated the relationship of the single nucleotide polymorphisms (SNPs), 2677G and 3435C, in the MDR1 gene and the effect of the anti-MDR1 single chain antibody (scAb) using pancreatic cancer cell lines.
We exposed the pancreatic cancer cell lines, AsCP-1, Panc-1, BxPC-3, MIAPaCa-2 and QGP-1 to 0.1-1,000µ g/mL of 5-FU for 72h and calculated the cytotoxic reactions. Combined therapy with an established anti-MDR1 neutralizing scAb and 10µg/mL of 5-FU was also performed.
AsCP-1 contained wild types of MDR1 2677G and 3435C, and showed the most 5-FU resistance. The anticancer effect of AsPC-1 increased with anti-MDR1 scAb, but the effect was not significant compared with other cell lines.
The cells with the wild type SNPs of MDR1 showed drug resistance, but we were not able to confirm a remarkable effect of the anti-MDR1 antibody.
Hepato-gastroenterology 07/2011; 59(113):272-5. · 0.66 Impact Factor
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ABSTRACT: At present, no effective chemotherapy for pancreatic neuroendocrine carcinoma (PNEC) exists. However, anti-angiogenic therapy is expected to be effective for PNEC, a hypervascular tumor. We treated PNEC and hypovascular pancreatic ductal cell carcinoma (DCC) cell lines with the anti-vascular endothelial growth factor (VEGF) antibody bevacizumab, and compared the antitumor effect between the two different types of cell lines. The PNEC cell line QGP-1 and the DCC cell lines BxPC-3 and AsPC-1 were used. We evaluated the ability of the cell lines to proliferate and secrete VEGF in vitro, the antitumor effect of bevacizumab administration in vivo and the side effects of bevacizumab on the pancreas in a caerulein-induced pancreatitis model. Comparison of the QGP-1 and DCC cell lines showed that QGP-1 secreted a higher level of VEGF under a hypoxic environment than the DCC cell line, and bevacizumab exerted the most marked growth-inhibitory effect on QGP-1; the number of intratumoral blood vessels decreased and the percentage of proliferating cells was approximately the same. In the pancreatitis model, bevacizumab administration did not adversely affect the pancreatitis or the associated hypoxic environment. Bevacizumab does not affect the pancreas itself; therefore, its potent inhibitory effect on the growth of pancreatic neuroendocrine tumors alone can be expected.
Experimental and therapeutic medicine 01/2011; 2(6):1047-1052.
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Kazuhiko Kasuya,
Takao Itoi,
Takaaki Matsudo,
Bunsoh Kyo,
Yasushi Endo,
Takahisa Ikeda, Yuichi Nagakawa,
Yoshiaki Suzuki,
Motohide Shimazu,
Tatsuya Aoki,
Akihiko Tsuchida
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ABSTRACT: We describe the surgical method of cases showing a distended gallbladder. Because the most important thing does not cause biliary tract injury, it is to find orientation carefully. The frequency of incidental gallbladder cancer was in 7 (0.7%) of the 983. Only cholecystectomy is necessary to be performed for Tis or T1 cancer, and surgery has to be changed to radical surgery for T2 cancer or deeper invasion. Laparoscopic cholecystectomy is already an established standard operation. In the presence of acute or severe chronic inflammation, special attention should be paid to these points.
ISRN surgery. 01/2011; 2011:827465.
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Kazuhiko Kasuya,
Katsutoshi Sugimoto,
Bunsoh Kyo, Yuichi Nagakawa,
Takahisa Ikeda,
Yasuharu Mori,
Tatehiko Wada,
Minako Suzuki,
Takeshi Nagai,
Takao Itoi,
Motohide Shimazu,
Tatsuya Aoki,
Akihiko Tsuchida
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ABSTRACT: For hepatic tumors that cannot be identified on routine ultrasonography (US), we marked the target area using real-time virtual sonography (RVS) with indocyanine green (ICG)-ethanol (1:100) during surgery, and performed hepatic resection while observing the fluorescence. EXPERIMENT: An ICG-ethanol mixture locally injected into mouse liver was retained in the same area for more than 4 h. The same mixture locally injected into pig liver at a depth of 3 cm could be observed using an infrared camera.
An ICG-ethanol mixture (500 μl) was locally injected under RVS guidance into a metastatic hepatic tumor that was visible only on magnetic resonance imaging (MRI), and hepatic resection was performed while Photodynamic Eye (PDE) images were being observed. The metastatic lesion (3 mm in diameter in a pathological specimen) could be successfully resected.
This method was useful for resecting US-invisible hepatic tumors.
Journal of hepato-biliary-pancreatic sciences. 12/2010; 18(3):380-5.
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Masatoshi Shigoka,
Akihiko Tsuchida,
Takaaki Matsudo, Yuichi Nagakawa,
Hitoshi Saito,
Yoshiaki Suzuki,
Tatsuya Aoki,
Yoshiki Murakami,
Hidenori Toyoda,
Takashi Kumada,
Ralf Bartenschlager,
Nobuyuki Kato,
Masanori Ikeda,
Tomoki Takashina,
Masami Tanaka,
Rieko Suzuki,
Kosuke Oikawa,
Masakatsu Takanashi,
Masahiko Kuroda
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ABSTRACT: MicroRNAs (miRNAs) belong to a class of the endogenously expressed non-coding small RNAs which primarily function as gene regulators. Growing evidence suggests that miRNAs have a significant role in tumor development and may constitute robust biomarkers for cancer diagnosis and prognosis. The miR-17-92 cluster especially is markedly overexpressed in several cancers, and is associated with the cancer development and progression. In this study, we have demonstrated that miR-92a is highly expressed in hepatocellular carcinoma (HCC). In addition, the proliferation of HCC-derived cell lines was enhanced by miR-92a and inhibited by the anti-miR-92a antagomir. On the other hand, we have found that the relative amount of miR-92a in the plasmas from HCC patients is decreased compared with that from the healthy donors. Interestingly, the amount of miR-92a was elevated after surgical treatment. Thus, although the physiological significance of the decrease of miR-92a in plasma is still unknown, deregulation of miR-92 expression in cells and plasma should be implicated in the development of HCC.
Pathology International 05/2010; 60(5):351-7. · 1.62 Impact Factor
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ABSTRACT: Pancreaticobiliary maljunction (PBM) is associated with the occurrence of biliary cancer due to pancreatobiliary reflux. We present a case of simultaneous double cancer of the gallbladder and bile duct. A 77-year-old woman who had jaundice, intra- and extra-hepatic biliary ductal dilatation and a space-occupying lesion in the gallbladder and lower bile duct underwent pancreatoduodenectomy. The gallbladder cancer showed papillary carcinoma without mutation of the K-ras gene and with p53 non-sense mutation of CCA (Pro) to CA (Stop) on codon 301 in exon 8. The bile duct cancer revealed a well-differentiated adenocarcinoma without mutation of the K-ras gene and with p53 miss-sense mutation of GTG (Val) to GAG (Glu) on codon 272 in exon 8. There were no mutations of either the K-ras or p53 gene in non-cancerous epithelia. In contrast, only the mucosa of the common channel had p53 protein accumulation and high cell proliferation activity. Therefore, the genetic pathway might be the same in both the gallbladder and bile duct cancer, and a high potential for carcinogenesis might be present in the epithelium of the common channel in patients with PBM.
Journal of Hepato-Biliary-Pancreatic Surgery 02/2009; 16(3):376-81. · 1.60 Impact Factor
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ABSTRACT: The VIO soft-coagulation system (SC) is a new device for tissue coagulation. We hypothesized that this device would be an effective tool for sealing small pancreatic ducts, thus reducing pancreatic fistula following pancreatectomy.
To confirm whether the SC could be used to seal small pancreatic ducts, we measured the burst pressure in sealed ducts in mongrel dogs. Eight dogs underwent distal pancreatectomy, with the remnant stump coagulated by using the SC. The animals were necropsied on postoperative day 10. In a clinical trial, 11 patients who underwent pancreatoduodenectomy with SC treatment (SC group), and 24 patients who underwent pancreatoduodenectomy without SC treatment (non-SC group) were compared.
In the experimental study, the burst-pressure test revealed that the SC had efficiently sealed the small pancreatic ducts. Histological examination revealed completely obstructed pancreatic ductal structures, ranging from large pancreatic ducts (diameter, 500 microm) to microscopic ducts. No pancreatic leakage was observed following distal pancreatectomy without main pancreatic duct (MPD) suturing in dogs that had an MPD diameter of less than 500 microm. In the clinical trial, pancreatic fistula developed in only one patient (9.1%) in the SC group, but a pancreatic fistula developed in five patients (20.8%) in the non-SC group.
This novel technique using the SC is an effective procedure for preventing the development of pancreatic fistula following pancreatectomy.
Journal of Hepato-Biliary-Pancreatic Surgery 02/2008; 15(4):359-65. · 1.60 Impact Factor
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ABSTRACT: The p53 tumor suppressor gene family consists of three genes, p53, p63, and p73. p53 family proteins share high homology in their DNA-binding domains but exhibit diverse biological functions. In this study, we demonstrated differential target gene activation by specific p53, p63, and p73 induction in Saos2 cells by oligonucleotide microarray expression analysis. We further analyzed the WNT4 promoter, which was induced by p63 and p73 but not p53, in order to clarify the mechanism of differential target gene activation between the three family members. Luciferase analysis showed that the WNT4 promoter harbors two p63/p73 response elements, designated RE1 and RE2. RE1 resembles the canonical p53 response element (tandem repeats of RRRCWWGYYY), located between -141 and -121, while RE2 consists of a GC-rich sequence further downstream. Neither response element alone was able to confer transcriptional activity. It is thus likely that both RE1 and RE2 are necessary in rendering p63/p73-specific activation of the WNT4 promoter.
Biochemical and Biophysical Research Communications 02/2006; 339(4):1120-8. · 2.48 Impact Factor
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ABSTRACT: p63, a member of the p53 superfamily, is an essential cell fate determinant for stratified epithelium. Deficiency of p63 leads to lack of differentiated epithelium from the skin and the presence of trace undifferentiated cells left in the dermis. We found that transcriptionally active isoforms of p63, TAp63beta and TAp63gamma, activated the skin-specific promoter of bullous pemphigoid antigen 1 (BPAG-1). The p63-response element was localized between bases -177 and -153 upstream of exon 1 in the BPAG-1e promoter, whereas regions surrounding the response element suppressed transcriptional responses to p53 and TAp73beta, resulting in p63-specific activation of the promoter. This represents a novel molecular mechanism by which target gene induction by p63 is distinguished from induction by other p53 family members.
Journal of Investigative Dermatology 08/2005; 125(1):52-60. · 6.31 Impact Factor
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ABSTRACT: An orthotopic liver transplant model in the rat was used to evaluate the role of tumor necrosis factor alpha (TNF-alpha) in liver transplant rejection. There were significantly increased levels of TNF-alpha mRNA and parallel increases in 8-hydroxy-2' deoxyguanosine (8-OHdG) indicative of oxidative DNA damage present 7 to 12 days after transplantation. Cells staining positively for 8-OHdG were localized to the cytoplasm of hepatocytes adjacent to the TNF-alpha expressing inflammatory cells in the portal areas or in patches surrounded by inflammatory cells in the hepatic sinusoids. Significantly more cells staining for 8-OHdG were found in the allogeneic grafts that were strongly rejected than in the syngeneic controls or in the grafts placed in species that accepted the allograft permanently after a rejection episode. TUNEL reactivity lagged 2 days behind peak reactivity for 8-OHdG. On day 12 after transplantation, many cells stained for both 8-OHdG and TUNEL, indicating that the cells suffering oxidative DNA injury were undergoing apoptosis or death. Oxidative injury resulted in mtDNA deletion consisting of 4,834 base-pairs. Studies of hepatocytes cultured from normal rats displayed dose-dependent relationships between TNF-alpha concentration and 8-OHdG and mtDNA mutation. Repetitive intraperitoneal injection of Enbrel, a TNF receptor blocker, significantly decreased hepatocyte 8-OHdG levels and the frequency of deleted mtDNA while greatly extending graft survival time. In conclusion, the data presented implicate TNF-alpha as being capable of causing oxidative DNA damage and mtDNA mutation in hepatocytes.
Hepatology 08/2005; 42(1):208-15. · 11.66 Impact Factor
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ABSTRACT: p63 is a member of the p53 tumor suppressor gene family, which regulates downstream target gene expression by binding to sequence-specific response elements similar to those of p53. By using oligonucleotide expression microarray analysis and analyzing the promoters of p63-induced genes, we have identified novel p63-specific response elements (p63-REs) in the promoter regions of EVPL and SMARCD3. These p63-REs exhibit characteristic differences from the canonical p53-RE (RRRCWWGYYY) in both the core-binding element (CWWG) as well as the RRR and/or YYY stretches. Luciferase assays on mutagenized promoter constructs followed by electromobility shift analysis showed that p53 preferentially activates and binds to the RRRCATGYYY sequence, whereas p63 preferentially activates RRRCGTGYYY. Whereas EVPL protein is highly expressed in epithelial cells of the skin and pharynx in the p63+/+ mouse, it is undetectable in these tissues in the p63-/- mouse. Our results indicate that p63 can regulate expression of specific target genes such as those involved in skin, limb, and craniofacial development by preferentially activating distinct p63-specific response elements.
Molecular and Cellular Biology 08/2005; 25(14):6077-89. · 5.53 Impact Factor
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ABSTRACT: Early and accurate detection of acute cellular rejection (ACR) is important in the management of liver allograft recipients. We hypothesized that expression of allograft inflammatory factor (AIF)-1 would be associated with liver allograft rejection as previous studies have shown that a relationship exists between kidney and heart transplantation. Indeed using rat orthotopic transplant models we found that the expression of allograft inflammatory factor-1 (AIF-1) can be detected in both allograft and peripheral blood leukocytes with peak levels detected 7 days following liver transplantation. Interestingly, AIF-1 expression increased 2-fold in acutely rejecting liver allografts compared to chronically accepted livers on days 5, 7 and 10 after transplantation. AIF-1 expression in peripheral blood leukocytes was also significantly greater in the rejection model than in the acceptance model. Flow cytometric analysis of peripheral blood leukocytes demonstrated that AIF-1 was expressed in ED2-positive cells, a marker for Kupffer cells. In vitro studies showed that AIF-1 expression in Kupffer cells was up-regulated by coculture with Th1 cytokines. However, neither LPS nor Escherichia coli (E. coli) administration had an affect on AIF-1 expression. These data indicate that high levels of AIF-1 expression reflect aggressive liver allograft rejection and suggest a role for monitoring AIF-1 in peripheral blood leukocytes as a monitor for increased immunosuppression.
American Journal of Transplantation 01/2005; 4(12):1949-57. · 6.39 Impact Factor
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ABSTRACT: Fas-Fas ligand (FasL)-dependent pathways exert a suppressive effect on inflammatory responses in immune-privileged organs. FasL expression in hepatic Kupffer cells (KC) has been implicated in hepatic immunoregulation. In this study, modulation of FasL expression of KC by endogenous gut-derived bacterial LPS and the role of reactive oxygen species (ROS) as potential mediators of FasL expression in KC were investigated. LPS stimulation of KC resulted in upstream ROS generation and, subsequently, increased FasL expression and consequent Jurkat cell (Fas-positive) apoptosis. The NADPH oxidase and xanthine oxidase enzymatic pathways appear to be major sources of this upstream ROS generation. Increased FasL expression was blocked by antioxidants and by enzymatic blocking of ROS generation. Exogenous administration of H2O2 stimulated KC FasL expression and subsequent Jurkat cell apoptosis. Intracellular endogenous ROS generation may therefore represent an important signal transduction pathway for FasL expression in KC.
AJP Gastrointestinal and Liver Physiology 10/2004; 287(3):G620-6. · 3.43 Impact Factor
