CEACAM1+ myeloid cells control angiogenesis in inflammation.

Standard

CEACAM1+ myeloid cells control angiogenesis in inflammation. / Horst, Andrea; Bickert, Thomas; Brewig, Nancy; Ludewig, Peter; van Rooijen, Nico; Schumacher, Udo; Beauchemin, Nicole; Ito, Wulf D; Fleischer, Bernhard; Wagener, Christoph; Ritter, Uwe.

in: BLOOD, Jahrgang 113, Nr. 26, 26, 2009, S. 6726-6736.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Horst, A, Bickert, T, Brewig, N, Ludewig, P, van Rooijen, N, Schumacher, U, Beauchemin, N, Ito, WD, Fleischer, B, Wagener, C & Ritter, U 2009, 'CEACAM1+ myeloid cells control angiogenesis in inflammation.', BLOOD, Jg. 113, Nr. 26, 26, S. 6726-6736. <http://www.ncbi.nlm.nih.gov/pubmed/19273835?dopt=Citation>

APA

Horst, A., Bickert, T., Brewig, N., Ludewig, P., van Rooijen, N., Schumacher, U., Beauchemin, N., Ito, W. D., Fleischer, B., Wagener, C., & Ritter, U. (2009). CEACAM1+ myeloid cells control angiogenesis in inflammation. BLOOD, 113(26), 6726-6736. [26]. http://www.ncbi.nlm.nih.gov/pubmed/19273835?dopt=Citation

Vancouver

Horst A, Bickert T, Brewig N, Ludewig P, van Rooijen N, Schumacher U et al. CEACAM1+ myeloid cells control angiogenesis in inflammation. BLOOD. 2009;113(26):6726-6736. 26.

Bibtex

@article{b460e5dd42d2475c948b7594468eaddb,
title = "CEACAM1+ myeloid cells control angiogenesis in inflammation.",
abstract = "Local inflammation during cutaneous leishmaniasis is accompanied by accumulation of CD11b(+) cells at the site of the infection. A functional role for these monocytic cells in local angiogenesis in leishmaniasis has not been described so far. Here, we show that CD11b(+) cells express high levels of the myeloid differentiation antigen carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1). In experimental cutaneous leishmaniasis in C57BL/6 wild-type (B6.WT) and B6.Ceacam1(-/-) mice, we found that only B6.Ceacam1(-/-) mice develop edemas and exhibit impairment of both hemangiogenesis and lymphangiogenesis. Because CEACAM1 expression correlates with functional angiogenesis, we further analyzed the role of the CD11b(+) population. In B6.Ceacam1(-/-) mice, we found systemic reduction of Ly-6C(high)/CD11b(high) monocyte precursors. To investigate whether CEACAM1(+) myeloid cells are causally related to efficient angiogenesis, we used reverse bone marrow transplants (BMTs) to restore CEACAM1(+) or CEACAM1(-) bone marrow in B6.Ceacam1(-/-) or B6.WT recipients, respectively. We found that angiogenesis was restored by CEACAM1(+) BMT only. In addition, we observed reduced morphogenic potential of inflammatory cells in Matrigel implants in CEACAM1(-) backgrounds or after systemic depletion of CD11b(high) macrophages. Taken together, we show for the first time that CEACAM1(+) myeloid cells are crucial for angiogenesis in inflammation.",
author = "Andrea Horst and Thomas Bickert and Nancy Brewig and Peter Ludewig and {van Rooijen}, Nico and Udo Schumacher and Nicole Beauchemin and Ito, {Wulf D} and Bernhard Fleischer and Christoph Wagener and Uwe Ritter",
year = "2009",
language = "Deutsch",
volume = "113",
pages = "6726--6736",
journal = "BLOOD",
issn = "0006-4971",
publisher = "American Society of Hematology",
number = "26",

}

RIS

TY - JOUR

T1 - CEACAM1+ myeloid cells control angiogenesis in inflammation.

AU - Horst, Andrea

AU - Bickert, Thomas

AU - Brewig, Nancy

AU - Ludewig, Peter

AU - van Rooijen, Nico

AU - Schumacher, Udo

AU - Beauchemin, Nicole

AU - Ito, Wulf D

AU - Fleischer, Bernhard

AU - Wagener, Christoph

AU - Ritter, Uwe

PY - 2009

Y1 - 2009

N2 - Local inflammation during cutaneous leishmaniasis is accompanied by accumulation of CD11b(+) cells at the site of the infection. A functional role for these monocytic cells in local angiogenesis in leishmaniasis has not been described so far. Here, we show that CD11b(+) cells express high levels of the myeloid differentiation antigen carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1). In experimental cutaneous leishmaniasis in C57BL/6 wild-type (B6.WT) and B6.Ceacam1(-/-) mice, we found that only B6.Ceacam1(-/-) mice develop edemas and exhibit impairment of both hemangiogenesis and lymphangiogenesis. Because CEACAM1 expression correlates with functional angiogenesis, we further analyzed the role of the CD11b(+) population. In B6.Ceacam1(-/-) mice, we found systemic reduction of Ly-6C(high)/CD11b(high) monocyte precursors. To investigate whether CEACAM1(+) myeloid cells are causally related to efficient angiogenesis, we used reverse bone marrow transplants (BMTs) to restore CEACAM1(+) or CEACAM1(-) bone marrow in B6.Ceacam1(-/-) or B6.WT recipients, respectively. We found that angiogenesis was restored by CEACAM1(+) BMT only. In addition, we observed reduced morphogenic potential of inflammatory cells in Matrigel implants in CEACAM1(-) backgrounds or after systemic depletion of CD11b(high) macrophages. Taken together, we show for the first time that CEACAM1(+) myeloid cells are crucial for angiogenesis in inflammation.

AB - Local inflammation during cutaneous leishmaniasis is accompanied by accumulation of CD11b(+) cells at the site of the infection. A functional role for these monocytic cells in local angiogenesis in leishmaniasis has not been described so far. Here, we show that CD11b(+) cells express high levels of the myeloid differentiation antigen carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1). In experimental cutaneous leishmaniasis in C57BL/6 wild-type (B6.WT) and B6.Ceacam1(-/-) mice, we found that only B6.Ceacam1(-/-) mice develop edemas and exhibit impairment of both hemangiogenesis and lymphangiogenesis. Because CEACAM1 expression correlates with functional angiogenesis, we further analyzed the role of the CD11b(+) population. In B6.Ceacam1(-/-) mice, we found systemic reduction of Ly-6C(high)/CD11b(high) monocyte precursors. To investigate whether CEACAM1(+) myeloid cells are causally related to efficient angiogenesis, we used reverse bone marrow transplants (BMTs) to restore CEACAM1(+) or CEACAM1(-) bone marrow in B6.Ceacam1(-/-) or B6.WT recipients, respectively. We found that angiogenesis was restored by CEACAM1(+) BMT only. In addition, we observed reduced morphogenic potential of inflammatory cells in Matrigel implants in CEACAM1(-) backgrounds or after systemic depletion of CD11b(high) macrophages. Taken together, we show for the first time that CEACAM1(+) myeloid cells are crucial for angiogenesis in inflammation.

M3 - SCORING: Zeitschriftenaufsatz

VL - 113

SP - 6726

EP - 6736

JO - BLOOD

JF - BLOOD

SN - 0006-4971

IS - 26

M1 - 26

ER -