At the dawn of inflammation: two ADAMs regulate extrapulmonary disease manifestations in pneumonia

<title>Extract</title> With 450 million cases per year, pneumonia is one of the most common diseases and is among the top five causes of mortality worldwide [1]. In addition to its direct impact on the lung and the associated morbidity and mortality, pneumonia is increasingly recognised for its pathogenic effects on extrapulmonary organs such as the heart, brain, kidney and blood vessels. As such, pneumonia is frequently associated with acute and chronic cardiovascular events, renal failure, or cognitive impairment [2]. The mechanisms underlying these extrapulmonary manifestations may involve systemic pathogen dissemination and formation of microlesions [3], as well as systemic inflammatory responses mediated by lung-derived pro-inflammatory cytokines, pathogen- or damage-associated molecular patterns, circulating immune cells or, notably, extracellular vesicles (EVs). These small, lipid bilayer-delimited particles are categorised based on size and mechanism of formation into exosomes, microvesicles and apoptotic bodies [4].