Introduction. Making work better.

From the premise that better work makes for better societies, the challenge, taken up in the introduction to this special issue of Transfer: European Review of Labour and Research, is to explore what makes work better, or worse, and how it can be improved. As a wide variety of experiments shape our economies and communities for the future, a key challenge is to engage in shared learning about these processes in order to stimulate a dialogue between the aspiration for better work and the conditions likely to hinder or facilitate making work better. It is an invitation to move from narrow conceptions of job quality to a broader lens of how world-of-work actors strategise, innovate and incorporate uncertainty into their search for sustainable solutions for better work. Key themes include: why work needs to be better (but is often worse); why better work makes for better societies; how work can be made better; the role of institutions in achieving better work; and, finally, how union strategies are essential to processes of experimentation to make work better.

An original infection model identifies host lipoprotein import as a route for blood-brain barrier crossing.

Pathogens able to cross the blood-brain barrier (BBB) induce long-term neurological sequelae and death. Understanding how neurotropic pathogens bypass this strong physiological barrier is a prerequisite to devise therapeutic strategies. Here we propose an innovative model of infection in the developing Drosophila brain, combining whole brain explants with in vivo systemic infection. We find that several mammalian pathogens are able to cross the Drosophila BBB, including Group B Streptococcus (GBS). Amongst GBS surface components, lipoproteins, and in particular the B leucine-rich Blr, are important for BBB crossing and virulence in Drosophila. Further, we identify (V)LDL receptor LpR2, expressed in the BBB, as a host receptor for Blr, allowing GBS translocation through endocytosis. Finally, we show that Blr is required for BBB crossing and pathogenicity in a murine model of infection. Our results demonstrate the potential of Drosophila for studying BBB crossing by pathogens and identify a new mechanism by which pathogens exploit the machinery of host barriers to generate brain infection.