File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Depletion of intestinal resident macrophages prevents ischaemia reperfusion injury in gut
  • Basic View
  • Metadata View
  • XML View
TitleDepletion of intestinal resident macrophages prevents ischaemia reperfusion injury in gut
 
AuthorsChen, Y1
Lui, VCH1
Rooijen, NV2
Tam, PKH1
 
Issue Date2004
 
PublisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/
 
CitationGut, 2004, v. 53 n. 12, p. 1772-1780 [How to Cite?]
DOI: http://dx.doi.org/10.1136/gut.2003.034868
 
AbstractBackground and aims: The cellular and molecular events involved in ischaemia reperfusion (IR) injury are complex and not fully understood. Previous studies have implicated polymorphonuclear neutrophils (PMN) as major inflammatory cells in IR injury. However, anti-PMN antiserum treatment offers only limited protection, indicating that other inflammatory cells are involved. We have therefore investigated the contribution of resident macrophages in IR injury using an IR gut injury model. Methods: DA rats were divided into sham operation and IR groups. The superior mesenteric artery was clamped for 30, 45, or 60 minutes (ischaemia) followed by 60 minutes of reperfusion. IR injuries were evaluated by histological staining. Expression of early growth response factor 1 (Egr-1), myeloperoxidase (MPO), and proinflammatory cytokines was analysed by immunohistochemistry, reverse transcription-polymerase chain reaction, and western blotting analysis. The specific role of macrophages in IR gut injury was also evaluated in resident macrophage depleted rats. Results: Mucosal sloughing and villi destruction were seen in 45/60 minute and 60/60 minute IR guts. PMN infiltration at the damaged mucosal area was undetectable in 45/60 minute and 60/60 minute IR guts. PMN were localised around the capillaries at the base of the crypts in 60/60 minute IR gut. Obvious PMN infiltration was only observed in damaged villi after three hours of reperfusion. Elevated nuclear Egr-1 immunostaining was localised in resident macrophages at the damaged villi before histological appearance of mucosal damage. Furthermore, resident macrophages at the damaged site expressed MPO. Protein levels of the proinflammatory cytokines RANTES and MCP-1 were increased in IR gut. Depletion of resident macrophages by dichloromethylene bisphosphonate significantly reduced mucosal damage in rat guts after IR. Conclusion: Our findings indicate that resident macrophages play a role in early mucosal damage in IR gut injury. Therefore, macrophages should be treated as a prime target for therapeutic intervention for IR damage.
 
ISSN0017-5749
2013 Impact Factor: 13.319
 
DOIhttp://dx.doi.org/10.1136/gut.2003.034868
 
PubMed Central IDPMC1774329
 
ISI Accession Number IDWOS:000225059900013
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorChen, Y
 
dc.contributor.authorLui, VCH
 
dc.contributor.authorRooijen, NV
 
dc.contributor.authorTam, PKH
 
dc.date.accessioned2007-03-23T04:47:46Z
 
dc.date.available2007-03-23T04:47:46Z
 
dc.date.issued2004
 
dc.description.abstractBackground and aims: The cellular and molecular events involved in ischaemia reperfusion (IR) injury are complex and not fully understood. Previous studies have implicated polymorphonuclear neutrophils (PMN) as major inflammatory cells in IR injury. However, anti-PMN antiserum treatment offers only limited protection, indicating that other inflammatory cells are involved. We have therefore investigated the contribution of resident macrophages in IR injury using an IR gut injury model. Methods: DA rats were divided into sham operation and IR groups. The superior mesenteric artery was clamped for 30, 45, or 60 minutes (ischaemia) followed by 60 minutes of reperfusion. IR injuries were evaluated by histological staining. Expression of early growth response factor 1 (Egr-1), myeloperoxidase (MPO), and proinflammatory cytokines was analysed by immunohistochemistry, reverse transcription-polymerase chain reaction, and western blotting analysis. The specific role of macrophages in IR gut injury was also evaluated in resident macrophage depleted rats. Results: Mucosal sloughing and villi destruction were seen in 45/60 minute and 60/60 minute IR guts. PMN infiltration at the damaged mucosal area was undetectable in 45/60 minute and 60/60 minute IR guts. PMN were localised around the capillaries at the base of the crypts in 60/60 minute IR gut. Obvious PMN infiltration was only observed in damaged villi after three hours of reperfusion. Elevated nuclear Egr-1 immunostaining was localised in resident macrophages at the damaged villi before histological appearance of mucosal damage. Furthermore, resident macrophages at the damaged site expressed MPO. Protein levels of the proinflammatory cytokines RANTES and MCP-1 were increased in IR gut. Depletion of resident macrophages by dichloromethylene bisphosphonate significantly reduced mucosal damage in rat guts after IR. Conclusion: Our findings indicate that resident macrophages play a role in early mucosal damage in IR gut injury. Therefore, macrophages should be treated as a prime target for therapeutic intervention for IR damage.
 
dc.description.naturepublished_or_final_version
 
dc.format.extent716934 bytes
 
dc.format.extent26112 bytes
 
dc.format.extent145392 bytes
 
dc.format.extent2666 bytes
 
dc.format.mimetypeapplication/pdf
 
dc.format.mimetypeapplication/msword
 
dc.format.mimetypeapplication/pdf
 
dc.format.mimetypetext/plain
 
dc.identifier.citationGut, 2004, v. 53 n. 12, p. 1772-1780 [How to Cite?]
DOI: http://dx.doi.org/10.1136/gut.2003.034868
 
dc.identifier.doihttp://dx.doi.org/10.1136/gut.2003.034868
 
dc.identifier.epage1780
 
dc.identifier.hkuros96649
 
dc.identifier.isiWOS:000225059900013
 
dc.identifier.issn0017-5749
2013 Impact Factor: 13.319
 
dc.identifier.issue12
 
dc.identifier.openurl
 
dc.identifier.pmcidPMC1774329
 
dc.identifier.pmid15542513
 
dc.identifier.scopuseid_2-s2.0-9344226823
 
dc.identifier.spage1772
 
dc.identifier.urihttp://hdl.handle.net/10722/43518
 
dc.identifier.volume53
 
dc.languageeng
 
dc.publisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofGut
 
dc.relation.referencesReferences in Scopus
 
dc.rightsGut. Copyright © B M J Publishing Group.
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshIntestinal mucosa - blood supply - pathology
 
dc.subject.meshMacrophages - metabolism - physiology
 
dc.subject.meshReperfusion injury - metabolism - pathology - prevention & control
 
dc.subject.meshRna, messenger - genetics
 
dc.subject.meshEarly growth response protein 1
 
dc.titleDepletion of intestinal resident macrophages prevents ischaemia reperfusion injury in gut
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Chen, Y</contributor.author>
<contributor.author>Lui, VCH</contributor.author>
<contributor.author>Rooijen, NV</contributor.author>
<contributor.author>Tam, PKH</contributor.author>
<date.accessioned>2007-03-23T04:47:46Z</date.accessioned>
<date.available>2007-03-23T04:47:46Z</date.available>
<date.issued>2004</date.issued>
<identifier.citation>Gut, 2004, v. 53 n. 12, p. 1772-1780</identifier.citation>
<identifier.issn>0017-5749</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/43518</identifier.uri>
<description.abstract>Background and aims: The cellular and molecular events involved in ischaemia reperfusion (IR) injury are complex and not fully understood. Previous studies have implicated polymorphonuclear neutrophils (PMN) as major inflammatory cells in IR injury. However, anti-PMN antiserum treatment offers only limited protection, indicating that other inflammatory cells are involved. We have therefore investigated the contribution of resident macrophages in IR injury using an IR gut injury model. Methods: DA rats were divided into sham operation and IR groups. The superior mesenteric artery was clamped for 30, 45, or 60 minutes (ischaemia) followed by 60 minutes of reperfusion. IR injuries were evaluated by histological staining. Expression of early growth response factor 1 (Egr-1), myeloperoxidase (MPO), and proinflammatory cytokines was analysed by immunohistochemistry, reverse transcription-polymerase chain reaction, and western blotting analysis. The specific role of macrophages in IR gut injury was also evaluated in resident macrophage depleted rats. Results: Mucosal sloughing and villi destruction were seen in 45/60 minute and 60/60 minute IR guts. PMN infiltration at the damaged mucosal area was undetectable in 45/60 minute and 60/60 minute IR guts. PMN were localised around the capillaries at the base of the crypts in 60/60 minute IR gut. Obvious PMN infiltration was only observed in damaged villi after three hours of reperfusion. Elevated nuclear Egr-1 immunostaining was localised in resident macrophages at the damaged villi before histological appearance of mucosal damage. Furthermore, resident macrophages at the damaged site expressed MPO. Protein levels of the proinflammatory cytokines RANTES and MCP-1 were increased in IR gut. Depletion of resident macrophages by dichloromethylene bisphosphonate significantly reduced mucosal damage in rat guts after IR. Conclusion: Our findings indicate that resident macrophages play a role in early mucosal damage in IR gut injury. Therefore, macrophages should be treated as a prime target for therapeutic intervention for IR damage.</description.abstract>
<format.extent>716934 bytes</format.extent>
<format.extent>26112 bytes</format.extent>
<format.extent>145392 bytes</format.extent>
<format.extent>2666 bytes</format.extent>
<format.mimetype>application/pdf</format.mimetype>
<format.mimetype>application/msword</format.mimetype>
<format.mimetype>application/pdf</format.mimetype>
<format.mimetype>text/plain</format.mimetype>
<language>eng</language>
<publisher>BMJ Publishing Group. The Journal&apos;s web site is located at http://gut.bmjjournals.com/</publisher>
<relation.ispartof>Gut</relation.ispartof>
<rights>Gut. Copyright &#169; B M J Publishing Group.</rights>
<rights>Creative Commons: Attribution 3.0 Hong Kong License</rights>
<subject.mesh>Intestinal mucosa - blood supply - pathology</subject.mesh>
<subject.mesh>Macrophages - metabolism - physiology</subject.mesh>
<subject.mesh>Reperfusion injury - metabolism - pathology - prevention &amp; control</subject.mesh>
<subject.mesh>Rna, messenger - genetics</subject.mesh>
<subject.mesh>Early growth response protein 1</subject.mesh>
<title>Depletion of intestinal resident macrophages prevents ischaemia reperfusion injury in gut</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=0017-5749&amp;volume=53&amp;issue=12&amp;spage=1772&amp;epage=1780&amp;date=2004&amp;atitle=Depletion+of+intestinal+resident+macrophages+prevents+ischaemia+reperfusion+injury+in+gut</identifier.openurl>
<description.nature>published_or_final_version</description.nature>
<identifier.doi>10.1136/gut.2003.034868</identifier.doi>
<identifier.pmid>15542513</identifier.pmid>
<identifier.pmcid>PMC1774329</identifier.pmcid>
<identifier.scopus>eid_2-s2.0-9344226823</identifier.scopus>
<identifier.hkuros>96649</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-9344226823&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>53</identifier.volume>
<identifier.issue>12</identifier.issue>
<identifier.spage>1772</identifier.spage>
<identifier.epage>1780</identifier.epage>
<identifier.isi>WOS:000225059900013</identifier.isi>
<publisher.place>United Kingdom</publisher.place>
<bitstream.url>http://hub.hku.hk/bitstream/10722/43518/1/96649.pdf</bitstream.url>
</item>
Author Affiliations
  1. The University of Hong Kong
  2. Vrije Universiteit Amsterdam