Editorial: Bacterial Effectors as Drivers of Human Disease: Models, Methods, Mechanisms

Abstract

Bacteria colonise virtually all ecological niches on earth. To interact with their surroundings, they evolved sophisticated multi-protein secretion systems that transport proteins, called effectors, from the bacterial cytoplasm into the extracellular space or directly into target bacteria or eukaryotic cells. Secretion systems therefore perform critical roles in inter-bacterial competition and the pathogenesis of many clinically important opportunistic and professional human pathogens. Generically numbered type I, type II, etc. secretion systems (T1SSs, T2SSs, …), the complex multi-protein architecture of each type is remarkably conserved in different bacteria (Costa et al., 2015). In contrast, the effector repertoires are diverse in numbers and composition reflecting adaptation to specific lifestyles. Environmental, broad host range pathogens like Legionella pneumophila encode more than 300 effectors (Qiu and Luo, 2017). These effectors, whilst not selected under evolutionary pressure by the human immune system, still allow L. pneumophila to cause opportunistic infections. In contrast, pathogens with a more restricted mammalian host range, such as Salmonella enterica, have a considerably smaller (~20-40) arsenal of effectors (Jennings et al., 2017). This Frontiers Research Topic comprises a series of reviews and original research articles highlighting common and pathogen-specific findings and approaches to dissect the function of effectors in bacterial pathogenesis.