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

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