Rethinking Volunteering and Cosmopolitanism: Beyond Individual Mobilities and Personal Transformations

In this paper we use assemblage thinking to offer a new interrogation of the relationalities of volunteering and development and to revisit volunteering’s relationship to cosmopolitanism. Recent debates about the rise of new actors in development cooperation have seen a growing interest in the geopolitical significance of volunteers and their contribution to development. Research has addressed the ways international volunteering can shape cosmopolitan subjectivities, whilst claims for volunteering’s universality are a key feature of global development policy. However, we argue that existing approaches to volunteering, cosmopolitanism and development remain contained by established development imaginaries and their ascription of agency, authority and expertise to actors from the global North. We use the idea of the assemblage, and data from two research projects, the International Federation of Red Cross and Red Crescent’s (IFRC) Global Review on Volunteering, and a doctoral research project on diaspora volunteering, to explore the constitution of what volunteering is within and between places. Through this, we identify alternative sites for interrogating the capacity of volunteering to challenge established ideas of agency, care and responsibility in development

Volunteering hierarchies in the global South: remuneration and livelihoods

This paper explores volunteering and inequality in the global South through an analysis of volunteering remuneration. We argue that the growing remuneration of volunteers reflects an increasing financialisation of volunteering by aid and development donors to match labour to project and sectoral objectives. We examine how these remuneration strategies shape volunteering economies and (re)produce hierarchies and inequalities in contexts in the global South where volunteers are often from marginalised communities. We analyse data collected in Africa and the Middle East as part of the International Federation of Red Cross and Red Crescent Societies (IFRC) ‘Global Review on Volunteering’ to explore these interweaving volunteering hierarchies and how they articulate with existing social stratifications. In these contexts, we argue that a livelihoods and capabilities approach across macro, national and local levels provides an alternative and more nuanced way of accounting for volunteer remuneration within the range of assets that communities have to build their lives and future. When oriented towards catalysing these community assets, and away from rewarding particular kinds of individual labour, remuneration has the potential to enable rather than undermine sustained volunteering activity by and within marginalised communities

Senescent cell-derived extracellular vesicles as potential mediators of innate immunosenescence and inflammaging

Ageing is accompanied by a decline in immune function (immunosenescence), increased inflammation (inflammaging), and more senescent cells which together contribute to age-related disease and infection susceptibility. The innate immune system is the front-line defence against infection and cancer and is also involved in the removal of senescent cells, so preventing innate immunosenescence and inflammaging is vital for health in older age. Extracellular vesicles (EVs) modulate many aspects of innate immune function, including chemotaxis, anti-microbial responses, and immune regulation. Senescent cell derived EVs (SEVs) have different cargo to that of non-senescent cell derived EVs, suggesting alterations in EV cargo across the lifespan may influence innate immune function, possibly contributing to immunosenescence and inflammaging. Here we review current understanding of the potential impact of miRNAs, lipids and proteins, found in higher concentrations in SEVs, on innate immune functions and inflammation to consider whether SEVs are potential influencers of innate immunosenescence and inflammaging. Furthermore, senolytics have demonstrated an ability to return plasma EV content closer to that of non-senescent EVs, therefore the potential use of senotherapeutics (senolytics and senostatics) to ameliorate the effects of SEVs on immunosenescence and inflammaging is also considered as a possible strategy for extending health-span in older adults

Dysregulated neutrophil phenotype and function in hospitalised non-ICU COVID-19 pneumonia

Rationale: Infection with the SARS-CoV2 virus is associated with elevated neutrophil counts. Evidence of neutrophil dysfunction in COVID-19 is based on transcriptomics or single functional assays. Cell functions are interwoven pathways, and understanding the effect across the spectrum of neutrophil function may identify therapeutic targets. Objectives: Examine neutrophil phenotype and function in 41 hospitalised, non-ICU COVID-19 patients versus 23 age-matched controls (AMC) and 26 community acquired pneumonia patients (CAP). Methods: Isolated neutrophils underwent ex vivo analyses for migration, bacterial phagocytosis, ROS generation, NETosis and receptor expression. Circulating DNAse 1 activity, levels of cfDNA, MPO, VEGF, IL-6 and sTNFRI were measured and correlated to clinical outcome. Serial sampling on day three to five post hospitalization were also measured. The effect of ex vivo PI3K inhibition was measured in a further cohort of 18 COVID-19 patients. Results: Compared to AMC and CAP, COVID-19 neutrophils demonstrated elevated transmigration (p = 0.0397) and NETosis (p = 0.0332), and impaired phagocytosis (p = 0.0036) associated with impaired ROS generation (p < 0.0001). The percentage of CD54+ neutrophils (p < 0.001) was significantly increased, while surface expression of CD11b (p = 0.0014) and PD-L1 (p = 0.006) were significantly decreased in COVID-19. COVID-19 and CAP patients showed increased systemic markers of NETosis including increased cfDNA (p = 0.0396) and impaired DNAse activity (p < 0.0001). The ex vivo inhibition of PI3K γ and δ reduced NET release by COVID-19 neutrophils (p = 0.0129). Conclusions: COVID-19 is associated with neutrophil dysfunction across all main effector functions, with altered phenotype, elevated migration and NETosis, and impaired antimicrobial responses. These changes highlight that targeting neutrophil function may help modulate COVID-19 severity