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Article: Shift of homeostasis from parenchymal regeneration to fibroblast proliferation induced by lipopolysaccharide-activated macrophages in gastric mucosal healing in vitro

TitleShift of homeostasis from parenchymal regeneration to fibroblast proliferation induced by lipopolysaccharide-activated macrophages in gastric mucosal healing in vitro
Authors
Issue Date2007
PublisherBlackwell Publishing, Inc. The Journal's web site is located at http://www.blackwellpublishing.com/journals/WRR
Citation
Wound Repair And Regeneration, 2007, v. 15 n. 2, p. 221-226 How to Cite?
AbstractWound healing in the gastrointestinal tract is an orderly process involving orchestrated responses of various cell types. Lipopolysaccharides (LPS) are major components of the outer membrane of Gram-negative bacteria, which are known to impair gastric ulcer healing in animals. The influence of LPS on intercellular communication in wound healing, however, is unknown. We examined the effects of LPS-induced macrophage activation on the proliferative response in cultured rat gastric epithelial cells (RGM-1) and fibroblasts JHU-25. Rat peritoneal resident macrophages were activated with increasing doses of LPS. The supernatant from the activated macrophage preparation, designated as macrophage-conditioned medium, was then used to treat RGM-1 or JHU-25 cells. Cell proliferation and migration were determined by [3H]-thymidine incorporation and a monolayer wound-healing assay, respectively. Macrophage-conditioned medium significantly suppressed RGM-1 cell proliferation but had no effect on cell migration. The same medium, however, increased JHU-25 cell proliferation. LPS treatment alone suppressed JHU-25 cell proliferation while it had no effect on RGM-1 cell proliferation, indicating that the differential effects of the macrophage-conditioned medium on cell proliferation were elicited by the factors derived from macrophages. In this regard, tumor necrosis factor (TNF)-α stimulated while interleukin (IL)-1β suppressed RGM-1 cell proliferation, suggesting that IL-1β but not TNF-α may play a part in the mediation of the antiproliferative effect of macrophage-conditioned medium on gastric epithelial cells. In contrast, IL-1β suppressed while TNF-α had no effect on JHU-25 cell proliferation. Collectively, LPS-activated macrophages delay gastric mucosal regeneration but promote fibroblast proliferation in vitro. Such changes may partly elucidate the detrimental effect of bacterial infection on tissue repair in the stomach. © 2007 by the Wound Healing Society.
Persistent Identifierhttp://hdl.handle.net/10722/80299
ISSN
2015 Impact Factor: 2.628
2015 SCImago Journal Rankings: 1.149
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKei Wu, WKen_HK
dc.contributor.authorYin Law, PTen_HK
dc.contributor.authorShan Wong, HPen_HK
dc.contributor.authorYee Lam, EKen_HK
dc.contributor.authorKi Tai, EKen_HK
dc.contributor.authorShin, VYen_HK
dc.contributor.authorCho, CHen_HK
dc.date.accessioned2010-09-06T08:04:46Z-
dc.date.available2010-09-06T08:04:46Z-
dc.date.issued2007en_HK
dc.identifier.citationWound Repair And Regeneration, 2007, v. 15 n. 2, p. 221-226en_HK
dc.identifier.issn1067-1927en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80299-
dc.description.abstractWound healing in the gastrointestinal tract is an orderly process involving orchestrated responses of various cell types. Lipopolysaccharides (LPS) are major components of the outer membrane of Gram-negative bacteria, which are known to impair gastric ulcer healing in animals. The influence of LPS on intercellular communication in wound healing, however, is unknown. We examined the effects of LPS-induced macrophage activation on the proliferative response in cultured rat gastric epithelial cells (RGM-1) and fibroblasts JHU-25. Rat peritoneal resident macrophages were activated with increasing doses of LPS. The supernatant from the activated macrophage preparation, designated as macrophage-conditioned medium, was then used to treat RGM-1 or JHU-25 cells. Cell proliferation and migration were determined by [3H]-thymidine incorporation and a monolayer wound-healing assay, respectively. Macrophage-conditioned medium significantly suppressed RGM-1 cell proliferation but had no effect on cell migration. The same medium, however, increased JHU-25 cell proliferation. LPS treatment alone suppressed JHU-25 cell proliferation while it had no effect on RGM-1 cell proliferation, indicating that the differential effects of the macrophage-conditioned medium on cell proliferation were elicited by the factors derived from macrophages. In this regard, tumor necrosis factor (TNF)-α stimulated while interleukin (IL)-1β suppressed RGM-1 cell proliferation, suggesting that IL-1β but not TNF-α may play a part in the mediation of the antiproliferative effect of macrophage-conditioned medium on gastric epithelial cells. In contrast, IL-1β suppressed while TNF-α had no effect on JHU-25 cell proliferation. Collectively, LPS-activated macrophages delay gastric mucosal regeneration but promote fibroblast proliferation in vitro. Such changes may partly elucidate the detrimental effect of bacterial infection on tissue repair in the stomach. © 2007 by the Wound Healing Society.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing, Inc. The Journal's web site is located at http://www.blackwellpublishing.com/journals/WRRen_HK
dc.relation.ispartofWound Repair and Regenerationen_HK
dc.titleShift of homeostasis from parenchymal regeneration to fibroblast proliferation induced by lipopolysaccharide-activated macrophages in gastric mucosal healing in vitroen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1067-1927&volume=15&spage=221&epage=226&date=2007&atitle=Shift+of+homeostasis+from+parenchymal+regeneration+to+fibroblast+proliferation+induced+by+lipopolysaccharide-activated+macrophages+in+gastric+mucosal+healing+in+vitroen_HK
dc.identifier.emailShan Wong, HP:hpswong@hkusua.hku.hken_HK
dc.identifier.authorityShan Wong, HP=rp00808en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1524-475X.2007.00208.xen_HK
dc.identifier.pmid17352754-
dc.identifier.scopuseid_2-s2.0-33847740353en_HK
dc.identifier.hkuros157309en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33847740353&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume15en_HK
dc.identifier.issue2en_HK
dc.identifier.spage221en_HK
dc.identifier.epage226en_HK
dc.identifier.isiWOS:000244741900008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridKei Wu, WK=16030879500en_HK
dc.identifier.scopusauthoridYin Law, PT=16032638700en_HK
dc.identifier.scopusauthoridShan Wong, HP=8644138100en_HK
dc.identifier.scopusauthoridYee Lam, EK=16032661400en_HK
dc.identifier.scopusauthoridKi Tai, EK=16031272700en_HK
dc.identifier.scopusauthoridShin, VY=7003491170en_HK
dc.identifier.scopusauthoridCho, CH=14067000400en_HK
dc.identifier.citeulike1152234-

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