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Article: The secreted Helicobacter cysteine-rich protein A causes adherence of human monocytes and differentiation into a macrophage-like phenotype

TitleThe secreted Helicobacter cysteine-rich protein A causes adherence of human monocytes and differentiation into a macrophage-like phenotype
Authors
KeywordsCytokine
Helicobacter pylori
Inflammation
Innate immunity
Macrophage
Monocyte
Pathogen/host interaction
Sel1-like repeat
Thp1
TPR
Issue Date2009
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/febslet
Citation
Febs Letters, 2009, v. 583 n. 10, p. 1637-1643 How to Cite?
AbstractHelicobacter pylori genomes typically contain 8 or 9 genes that code for secreted and highly disulfide-bridged proteins designated Helicobacter cysteine-rich proteins (Hcp). Here we show that HcpA (hp0211) but not HcpC (hp1098) triggers the differentiation of human myeloid Thp1 monocytes into macrophages. Small amounts of HcpA cause the transition of round-shaped monocytes into cells with star-like morphologies, adherence to the culture dish surface, phagocytosis of opsonized fluorescent microspheres, and expression of the surface marker protein CD11b, all of which are indicative of a macrophage-like phenotype. We conclude that HcpA acts as a bacterial immune modulator similar to a eukaryotic cytokine. © 2009 Federation of European Biochemical Societies.
Persistent Identifierhttp://hdl.handle.net/10722/168376
ISSN
2021 Impact Factor: 3.864
2020 SCImago Journal Rankings: 1.593
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDumrese, Cen_US
dc.contributor.authorSlomianka, Len_US
dc.contributor.authorZiegler, Uen_US
dc.contributor.authorChoi, SSen_US
dc.contributor.authorKalia, Aen_US
dc.contributor.authorFulurija, Aen_US
dc.contributor.authorLu, Wen_US
dc.contributor.authorBerg, DEen_US
dc.contributor.authorBenghezal, Men_US
dc.contributor.authorMarshall, Ben_US
dc.contributor.authorMittl, PREen_US
dc.date.accessioned2012-10-08T03:18:09Z-
dc.date.available2012-10-08T03:18:09Z-
dc.date.issued2009en_US
dc.identifier.citationFebs Letters, 2009, v. 583 n. 10, p. 1637-1643en_US
dc.identifier.issn0014-5793en_US
dc.identifier.urihttp://hdl.handle.net/10722/168376-
dc.description.abstractHelicobacter pylori genomes typically contain 8 or 9 genes that code for secreted and highly disulfide-bridged proteins designated Helicobacter cysteine-rich proteins (Hcp). Here we show that HcpA (hp0211) but not HcpC (hp1098) triggers the differentiation of human myeloid Thp1 monocytes into macrophages. Small amounts of HcpA cause the transition of round-shaped monocytes into cells with star-like morphologies, adherence to the culture dish surface, phagocytosis of opsonized fluorescent microspheres, and expression of the surface marker protein CD11b, all of which are indicative of a macrophage-like phenotype. We conclude that HcpA acts as a bacterial immune modulator similar to a eukaryotic cytokine. © 2009 Federation of European Biochemical Societies.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/febsleten_US
dc.relation.ispartofFEBS Lettersen_US
dc.subjectCytokine-
dc.subjectHelicobacter pylori-
dc.subjectInflammation-
dc.subjectInnate immunity-
dc.subjectMacrophage-
dc.subjectMonocyte-
dc.subjectPathogen/host interaction-
dc.subjectSel1-like repeat-
dc.subjectThp1-
dc.subjectTPR-
dc.subject.meshBacterial Proteins - Metabolismen_US
dc.subject.meshCell Adhesionen_US
dc.subject.meshCell Differentiationen_US
dc.subject.meshHelicobacter Pylori - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshMacrophages - Cytology - Metabolismen_US
dc.subject.meshMicroscopy, Electron, Scanningen_US
dc.subject.meshMonocytes - Cytology - Metabolismen_US
dc.subject.meshPhagocytosisen_US
dc.subject.meshPhenotypeen_US
dc.subject.meshRecombinant Proteins - Genetics - Metabolismen_US
dc.subject.meshBeta-Lactamases - Metabolismen_US
dc.titleThe secreted Helicobacter cysteine-rich protein A causes adherence of human monocytes and differentiation into a macrophage-like phenotypeen_US
dc.typeArticleen_US
dc.identifier.emailLu, W:luwei@hku.hken_US
dc.identifier.authorityLu, W=rp00754en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.febslet.2009.04.027en_US
dc.identifier.pmid19393649-
dc.identifier.scopuseid_2-s2.0-65549090576en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-65549090576&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume583en_US
dc.identifier.issue10en_US
dc.identifier.spage1637en_US
dc.identifier.epage1643en_US
dc.identifier.isiWOS:000266402500014-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridDumrese, C=8260347700en_US
dc.identifier.scopusauthoridSlomianka, L=6701607694en_US
dc.identifier.scopusauthoridZiegler, U=7006124035en_US
dc.identifier.scopusauthoridChoi, SS=15031343000en_US
dc.identifier.scopusauthoridKalia, A=7005451652en_US
dc.identifier.scopusauthoridFulurija, A=6602613332en_US
dc.identifier.scopusauthoridLu, W=27868087600en_US
dc.identifier.scopusauthoridBerg, DE=7202401139en_US
dc.identifier.scopusauthoridBenghezal, M=6603042586en_US
dc.identifier.scopusauthoridMarshall, B=7202280032en_US
dc.identifier.scopusauthoridMittl, PRE=6701704224en_US
dc.identifier.issnl0014-5793-

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