Listeria monocytogenes is a foodborne pathogen that could cause severe infection in the central nervous system of humans and animals. However, the molecular mechanism of the pathogenesis is not fundamentally assessed. This study aimed to analyze the role of reactive oxygen species (ROS) in L. monocytogenes during its invasion into glia cells. The ROS level in L. monocytogenes was manipulated using NAD(P)H oxidase inhibitor diphenyleneiodonium chloride (DPI) and ROS scavenger N-acetyl cysteine (NAC). Results showed that the invasiveness of L. monocytogenes was elevated when ROS was downregulated by DPI and NAC treatment. Expression profiles of proinflammatory factors in glia cells were also examined because they play important roles in the functions of glia cells in the brain immune system. The expression levels of proinflammatory factors (tumor necrosis factor α and interleukin-1β) in host glia cells were downregulated when invaded by L. monocytogenes with lower ROS level. This finding indicates that ROS may function as negative regulator during the invasion of L. monocytogenes in brain infection.
Keywords: Listeria monocytogenes; astrocytes; brain infection; invasion; reactive oxygen species.
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