Open AccessReprogramming of myeloid angiogenic cells by B artonella henselae leads to microenvironmental regulation of pathological angiogenesis
Author(s) -
O'Rourke Fiona,
Mändle Tanja,
Urbich Carmen,
Dimmeler Stefanie,
Michaelis U. Ruth,
Brandes Ralf P.,
Flötenmeyer Matthias,
Döring Claudia,
Hansmann MartinLeo,
Lauber Kirsten,
Ballhorn Wibke,
Kempf Volkhard A.J.
Publication year - 2015
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12447
Subject(s) - biology , angiogenesis , bacillary angiomatosis , bartonella henselae , myeloid , tumor microenvironment , immune system , cancer research , immunology , serology , antibody
Summary The contribution of myeloid cells to tumour microenvironments is a decisive factor in cancer progression. Tumour‐associated macrophages ( TAM s) 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 B artonella henselae , a bacterial pathogen causing vasculoproliferative diseases (bacillary angiomatosis), reprogrammes human myeloid angiogenic cells ( MAC s), 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 M 2 macrophage polarization. MAC s infected with B . henselae incorporated into endothelial sprouts and increased angiogenic growth. Infected MAC s 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.