Sneaky Serratia
Monday, August 29th, 2011
Many years ago in microbiology practical classes, we used to encourage students to smear bright red Serratia marcescens bacteria all over their hands so we could demonstrate principles of epidemiology and the spread of infection. At the time, this was believed to be a harmless marine bacterium, but we stopped when it gradually realised that this bug is not as harmless as we used to think. S. marcescens has been in the news recently as the cause of the highly contagious white pox disease which kills corals, but it has a wide host range that includes plants, insects and nematodes, and it is also an opportunistic pathogen of mammals including humans. A new paper in PLoS ONE reveals the way in which this bacterium invades human cells.
Serratia marcescens Is Able to Survive and Proliferate in Autophagic-Like Vacuoles inside Non-Phagocytic Cells. 2011 PLoS ONE 6(8): e24054. doi:10.1371/journal.pone.0024054
Serratia marcescens is an opportunistic human pathogen that represents a growing problem for public health, particularly in hospitalized or immunocompromised patients. However, little is known about factors and mechanisms that contribute to S. marcescens pathogenesis within its host. In this work, we explore the invasion process of this opportunistic pathogen to epithelial cells. We demonstrate that once internalized, Serratia is able not only to persist but also to multiply inside a large membrane-bound compartment. This structure displays autophagic-like features, acquiring LC3 and Rab7, markers described to be recruited throughout the progression of antibacterial autophagy. The majority of the autophagic-like vacuoles in which Serratia resides and proliferates are non-acidic and have no degradative properties, indicating that the bacteria are capable to either delay or prevent fusion with lysosomal compartments, altering the expected progression of autophagosome maturation. In addition, our results demonstrate that Serratia triggers a non-canonical autophagic process before internalization. These findings reveal that S. marcescens is able to manipulate the autophagic traffic, generating a suitable niche for survival and proliferation inside the host cell.
