The mechanics of housing collectivism: How forms and functions affect affordability

In countries worldwide, limited access to affordable housing is fuelling interest in collectivist solutions. Different organizational models are being developed to enable groups of people to own and control housing collectively. The benefits of such models have been widely promoted, not least in terms of delivering enhanced housing affordability for residents. However, evidence to support such claims is scarce and it remains unclear whether affordability is the product of collective forms and functions, or some other factor(s). To address this gap in knowledge, the paper presents findings from three case studies of English and Canadian housing collectives. Applying realist theories of causation, the processes affecting housing affordability are explained, conceptualizing two causal mechanisms which depict how organizational form, internal rules and regulatory activity, along with the unique role of the resident-owner, influence the setting of rents and prices. Further research is required to understand the prevalence of these mechanisms and their general application

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

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