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Cell Microbiol. 2015 Oct;17(10):1447-63. doi: 10.1111/cmi.12447. Epub 2015 May 19.

Reprogramming of myeloid angiogenic cells by Bartonella henselae leads to microenvironmental regulation of pathological angiogenesis.

Author information

1
Institute for Medical Microbiology and Infection Control, Goethe University, Frankfurt am Main, Germany.
2
Institute for Medical Microbiology and Infection Control, Eberhard Karls University, Tübingen, Germany.
3
Institute for Cardiovascular Regeneration, Goethe University, Frankfurt am Main, Germany.
4
Institute for Cardiovascular Physiology, Goethe University, Frankfurt am Main, Germany.
5
Department for Electronmicroscopy, Max Planck Institute for Developmental Biology, Tübingen, Germany.
6
Dr. Senckenberg Institute for Pathology, Goethe University, Frankfurt am Main, Germany.
7
Department of Radiation Oncology, Ludwig Maximilian University, Munich, Germany.

Abstract

The contribution of myeloid cells to tumour microenvironments is a decisive factor in cancer progression. Tumour-associated macrophages (TAMs) mediate tumour invasion and angiogenesis through matrix remodelling, immune modulation and release of pro-angiogenic cytokines. Nothing is known about how pathogenic bacteria affect myeloid cells in these processes. Here we show that Bartonella henselae, a bacterial pathogen causing vasculoproliferative diseases (bacillary angiomatosis), reprogrammes human myeloid angiogenic cells (MACs), a pro-angiogenic subset of circulating progenitor cells, towards a TAM-like phenotype with increased pro-angiogenic capacity. B. henselae infection resulted in inhibition of cell death, activation of angiogenic cellular programmes and induction of M2 macrophage polarization. MACs infected with B. henselae incorporated into endothelial sprouts and increased angiogenic growth. Infected MACs developed a vascular mimicry phenotype in vitro, and expression of B. henselae adhesin A was essential in inducing these angiogenic effects. Secretome analysis revealed that increased pro-angiogenic activities were associated with the creation of a tumour-like microenvironment dominated by angiogenic inflammatory cytokines and matrix remodelling compounds. Our results demonstrate that manipulation of myeloid cells by pathogenic bacteria can contribute to microenvironmental regulation of pathological tissue growth and suggest parallels underlying both bacterial infections and cancer.

PMID:
25857345
DOI:
10.1111/cmi.12447
[Indexed for MEDLINE]

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