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

Claudia Dumrese; Lutz Slomianka; Urs Ziegler; Sung Sook Choi; Awdhesh Kalia; Alma Fulurija; Wei Lu; Douglas E. Berg; Mohammed Benghezal; Barry Marshall; Peer R.E. Mittl

doi:10.1016/j.febslet.2009.04.027

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

Claudia Dumrese, Lutz Slomianka, Urs Ziegler, Sung Sook Choi, Awdhesh Kalia, Alma Fulurija, Wei Lu, Douglas E. Berg, Mohammed Benghezal, Barry Marshall, Peer R.E. Mittl

Research output: Contribution to journal › Article › peer-review

38 Scopus citations

Abstract

Helicobacter 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.

Original language	English (US)
Pages (from-to)	1637-1643
Number of pages	7
Journal	FEBS Letters
Volume	583
Issue number	10
DOIs	https://doi.org/10.1016/j.febslet.2009.04.027
State	Published - May 19 2009
Externally published	Yes

Keywords

Cytokine
Helicobacter pylori
Inflammation
Innate immunity
Macrophage
Monocyte
Pathogen/host interaction
Sel1-like repeat
TPR
Thp1

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/j.febslet.2009.04.027

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Dumrese, C., Slomianka, L., Ziegler, U., Choi, S. S., Kalia, A., Fulurija, A., Lu, W., Berg, D. E., Benghezal, M., Marshall, B., & Mittl, P. R. E. (2009). The secreted Helicobacter cysteine-rich protein A causes adherence of human monocytes and differentiation into a macrophage-like phenotype. FEBS Letters, 583(10), 1637-1643. https://doi.org/10.1016/j.febslet.2009.04.027

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title = "The secreted Helicobacter cysteine-rich protein A causes adherence of human monocytes and differentiation into a macrophage-like phenotype",

abstract = "Helicobacter 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.",

keywords = "Cytokine, Helicobacter pylori, Inflammation, Innate immunity, Macrophage, Monocyte, Pathogen/host interaction, Sel1-like repeat, TPR, Thp1",

author = "Claudia Dumrese and Lutz Slomianka and Urs Ziegler and Choi, {Sung Sook} and Awdhesh Kalia and Alma Fulurija and Wei Lu and Berg, {Douglas E.} and Mohammed Benghezal and Barry Marshall and Mittl, {Peer R.E.}",

note = "Funding Information: We would like to thank Klaus Marquardt for electron microscopy sample preparation and Prof. J. Fritz-Steuber for fruitful discussions. This work was supported by grants from the Velux Foundation (Z{\"u}rich, Switzerland) and the US National Institutes of Health (RO1 DK63041). Author contribution: C.D., flow-cytometry; L.S., light microscopy; U.Z., scanning electron microscopy; S.S.C., A.K., D.B., prepared mutant; A.F., W.L., M.B., B.M., analysed mutant in mice; P.R.E.M., designed study, protein and cell biology, wrote manuscript. ",

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T1 - The secreted Helicobacter cysteine-rich protein A causes adherence of human monocytes and differentiation into a macrophage-like phenotype

AU - Dumrese, Claudia

AU - Slomianka, Lutz

AU - Ziegler, Urs

AU - Choi, Sung Sook

AU - Kalia, Awdhesh

AU - Fulurija, Alma

AU - Lu, Wei

AU - Berg, Douglas E.

AU - Benghezal, Mohammed

AU - Marshall, Barry

AU - Mittl, Peer R.E.

N1 - Funding Information: We would like to thank Klaus Marquardt for electron microscopy sample preparation and Prof. J. Fritz-Steuber for fruitful discussions. This work was supported by grants from the Velux Foundation (Zürich, Switzerland) and the US National Institutes of Health (RO1 DK63041). Author contribution: C.D., flow-cytometry; L.S., light microscopy; U.Z., scanning electron microscopy; S.S.C., A.K., D.B., prepared mutant; A.F., W.L., M.B., B.M., analysed mutant in mice; P.R.E.M., designed study, protein and cell biology, wrote manuscript.

PY - 2009/5/19

Y1 - 2009/5/19

N2 - Helicobacter 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.

AB - Helicobacter 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.

KW - Cytokine

KW - Helicobacter pylori

KW - Inflammation

KW - Innate immunity

KW - Macrophage

KW - Monocyte

KW - Pathogen/host interaction

KW - Sel1-like repeat

KW - TPR

KW - Thp1

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ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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