Absence of core autophagy gene expression in an ex vivo central nervous system model infected with Listeria monocytogenes

Recent studies have suggested that autophagy can act as a protective immune mechanism against Listeria monocytogenes infection. L. monocytogenes is a Gram-positive, facultative intracellular bacterium that causes invasive diseases in humans and animals, particularly in the central nervous system (CNS). Human listeriosis of the CNS can manifest in many ways, including meningitis and brain abscesses. The initial line of defence against bacterial colonisation is provided by microglia, resident phagocytes of the CNS parenchyma. Microglial cells are also well known for clearing dead and dying neural cells after injury, and therefore play a key role in infectious diseases and neurodegeneration.

Little is known about the role of the autophagy pathway in host–pathogen interactions in the brain as most in vitro studies have used macrophages or epithelial cells to study this interaction. In the present work, a quantitative real time-PCR array analysis was performed to assess autophagy-related gene expression in a brain rat ex vivo organotypic nervous system model during L. monocytogenes infection. We found that, in brief, core autophagy gene expression is not modulated by the infection, despite the presence of intense microglial phagocytic activity on the brain tissue surface that can be seen by scanning electron microscopy. We conclude that, in our model, autophagy could play a role in homeostasis in the damaged brain tissue instead of an immune-relevant pathway.