File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Macrophage migration inhibitory factor expression correlates with inflammatory changes in human chronic hepatitis B infection

TitleMacrophage migration inhibitory factor expression correlates with inflammatory changes in human chronic hepatitis B infection
Authors
KeywordsHBV
Hepatic injury
Inflammation
MIF
Issue Date2005
PublisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1478-3223&site=1
Citation
Liver International, 2005, v. 25 n. 3, p. 571-579 How to Cite?
AbstractBackground: Macrophage migration inhibitory factor (MIF) has emerged to be a pivotal cytokine in immune-mediated diseases. Patients and methods: To investigate the role of MIF in chronic hepatitis B infection, we studied two groups of hepatitis B surface antigen positive patients: group 1 (immune tolerant, n = 16) and group 2 (immune clearance, n = 16). Serum level of MIF was measured by enzyme-linked immunosorbent assay and intrahepatic expression of MIF, macrophage and T-cell localisation were detected by double immunohistochemistry. Results: An increased serum MIF correlated significantly with increased serum alanine aminotransferase activity (r = 0.73, P < 0.001) and the severity of necroinflammatory injury (r = 0.642, P < 0.001). In group 2, there was marked MIF mRNA expression in all KP-1+ macrophages and CD45RO+ activated T cells and, to a lesser extent, in hepatocytes within inflammatory areas. In contrast to its mRNA expression, the cytoplasmic MIF protein level in hepatocytes, infiltrating macrophages and T cells within the inflammatory area was reduced, which probably contributed to the increased serum MIF level. Conclusions: Our data suggested that MIF played a role in sustaining cell-mediated hepatic injury during the immune-clearance phase of chronic hepatitis B infection. © Blackwell Munksgaard 2005.
Persistent Identifierhttp://hdl.handle.net/10722/83718
ISSN
2015 Impact Factor: 4.47
2015 SCImago Journal Rankings: 1.677
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, HYen_HK
dc.contributor.authorNanji, AAen_HK
dc.contributor.authorLuk, JMen_HK
dc.contributor.authorHuang, XRen_HK
dc.contributor.authorLo, CMen_HK
dc.contributor.authorChen, YXen_HK
dc.contributor.authorYuen, STen_HK
dc.contributor.authorLan, HYen_HK
dc.contributor.authorLau, GKKen_HK
dc.date.accessioned2010-09-06T08:44:23Z-
dc.date.available2010-09-06T08:44:23Z-
dc.date.issued2005en_HK
dc.identifier.citationLiver International, 2005, v. 25 n. 3, p. 571-579en_HK
dc.identifier.issn1478-3223en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83718-
dc.description.abstractBackground: Macrophage migration inhibitory factor (MIF) has emerged to be a pivotal cytokine in immune-mediated diseases. Patients and methods: To investigate the role of MIF in chronic hepatitis B infection, we studied two groups of hepatitis B surface antigen positive patients: group 1 (immune tolerant, n = 16) and group 2 (immune clearance, n = 16). Serum level of MIF was measured by enzyme-linked immunosorbent assay and intrahepatic expression of MIF, macrophage and T-cell localisation were detected by double immunohistochemistry. Results: An increased serum MIF correlated significantly with increased serum alanine aminotransferase activity (r = 0.73, P < 0.001) and the severity of necroinflammatory injury (r = 0.642, P < 0.001). In group 2, there was marked MIF mRNA expression in all KP-1+ macrophages and CD45RO+ activated T cells and, to a lesser extent, in hepatocytes within inflammatory areas. In contrast to its mRNA expression, the cytoplasmic MIF protein level in hepatocytes, infiltrating macrophages and T cells within the inflammatory area was reduced, which probably contributed to the increased serum MIF level. Conclusions: Our data suggested that MIF played a role in sustaining cell-mediated hepatic injury during the immune-clearance phase of chronic hepatitis B infection. © Blackwell Munksgaard 2005.en_HK
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1478-3223&site=1en_HK
dc.relation.ispartofLiver Internationalen_HK
dc.subjectHBVen_HK
dc.subjectHepatic injuryen_HK
dc.subjectInflammationen_HK
dc.subjectMIFen_HK
dc.titleMacrophage migration inhibitory factor expression correlates with inflammatory changes in human chronic hepatitis B infectionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1478-3223&volume=25&issue=3&spage=571&epage=579&date=2005&atitle=Macrophage+migration+inhibitory+factor+expression+correlates+with+inflammatory+changes+in+human+chronic+hepatitis+B+infectionen_HK
dc.identifier.emailLuk, JM: jmluk@hkucc.hku.hken_HK
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hken_HK
dc.identifier.authorityLuk, JM=rp00349en_HK
dc.identifier.authorityLo, CM=rp00412en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1478-3231.2005.01047.xen_HK
dc.identifier.pmid15910495-
dc.identifier.scopuseid_2-s2.0-20844446169en_HK
dc.identifier.hkuros99899en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-20844446169&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue3en_HK
dc.identifier.spage571en_HK
dc.identifier.epage579en_HK
dc.identifier.isiWOS:000229781700016-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZhang, HY=8965962000en_HK
dc.identifier.scopusauthoridNanji, AA=35885060300en_HK
dc.identifier.scopusauthoridLuk, JM=7006777791en_HK
dc.identifier.scopusauthoridHuang, XR=7410248090en_HK
dc.identifier.scopusauthoridLo, CM=7401771672en_HK
dc.identifier.scopusauthoridChen, YX=16416830300en_HK
dc.identifier.scopusauthoridYuen, ST=7103160927en_HK
dc.identifier.scopusauthoridLan, HY=7102710832en_HK
dc.identifier.scopusauthoridLau, GKK=7102301257en_HK
dc.identifier.citeulike205879-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats