A growing literature demonstrates that the pattern of anti-inflammatory mediators released is specific for the inflammatory lung environment encountered and is mediated through differential activation of damage- and pathogen-associated molecular pathogen receptors expressed on MSC surfaces [12]. This includes Toll-like receptors (TLRs) that are activated by viral RNA (e.g. TLR3) (as in COVID-19) and viral unmethylated CpG-DNA (e.g. TLR9), leading to downstream cell signalling pathways resulting in MSC activation [13]. MSC-secreted angiopoietin-1 (Ang-1) and keratinocyte growth factor (KGF) contribute to the restoration of alveolar–capillary barriers disrupted as part of ARDS pathogenesis [14], while specific inhibitory microRNAs in extracellular vesicles are also described as mediating the protective effects of MSCs in pre-clinical models of bacterial or non-infectious acute lung injuries [15].