Project description:Mycobacterium ulcerans is the causal agent of Buruli ulcer, a chronic infectious disease and the third most common mycobacterial disease worldwide. Without early treatment, M. ulcerans provokes massive skin ulcers, caused by the mycolactone toxin, its main virulence factor. However, spontaneous healing may occur in Buruli ulcer patients several months or years after the disease onset. We have shown, in an original mouse model, that bacterial load remains high and viable in spontaneously healed tissues, suggesting that M. ulcerans switches to low levels of mycolactone production, adapting its strategy to survive in such a hostile environment. We investigated the regulation of mycolactone production, by using an RNA-seq strategy to study bacterial adaptation within our original mouse model of spontaneous healing. Pathway analysis and characterization of the tissue environment showed that the bacillus adapted to its new environment by modifying its metabolic activity and switching nutrient sources. Thus, M. ulcerans ensures its survival in healing tissues by reducing its secondary metabolism, leading to an inhibition of mycolactone synthesis and changes in cell wall composition. These findings shed new light on mycolactone regulation and pave the way for new therapeutic strategies.
Project description:Fusobacterium nucleatum-treated LoVo cells reported an increased promoting CRC metastasis effect compared with PBS control. To understand the underlying mechanisms of Fusobacterium nucleatum-induced metastasis ability of CRC cells, we performed RNA-sequencing in LoVo cells s with or without Fusobacterium nucleatum treatment with three independent biological replicates.
