Global expression profile of Enterohemorrhagic Escherichia coli O157:H7 in phagosome of murine macrophages

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Dades bibliogràfiques
Publicat a:	bioRxiv (Jan 4, 2025)
Autor principal:	Riviere, Nahuel Agustin
Altres autors:	Jiang, Lin, Wu, Xiuju, Casabonne, Maria Carolina, Guo, Lu, Libia Yael Smith, Wanderson Marques Da Silva, Cataldi, Angel Adrian, Xing, Ke, Bei, Jinlong, Larzabal, Mariano
Publicat:	Cold Spring Harbor Laboratory Press
Matèries:	Shiga toxin Hemolytic uremic syndrome SOS response DNA biosynthesis Amino acids Oxidative stress Biosynthesis DNA damage Virulence Flagella Nitric oxide Cellular stress response Macrophages Detoxification Hydrogen peroxide
Accés en línia:	Citation/Abstract Full text outside of ProQuest
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Descripció
Resum:	EHEC O157:H7 is responsible for Hemolytic Uremic Syndrome (HUS) outbreaks in humans and its virulence is associated with Shiga toxin (Stx). During the pathogenesis of HUS, EHEC O157:H7 is phagocytized by the intestinal host macrophage into the phagosome. According to our study, a low percentage of phagocytized bacteria survived in the murine macrophage phagosome. To understand the initials mechanisms involved in bacterial persistence, we performed a global profile of bacterial RNAseq analysis in the early phagosome of murine macrophage and in vitro assays with more extreme stress conditions. The defense strategy of an early murine phagosome consisted on producing DNA damage, membrane damage, acid pH and nitric oxide (NO) agents. These hostile conditions triggering the bacterial SOS response, lipid biosynthesis and NO detoxification enzymes in response to DNA damage, membrane damage and nitric oxide agents, respectively. In turn, to survive, the bacterium conserves energy by downregulating flagellar biosynthesis, T3SS and T6SS virulence mechanisms. In contrast, stx2a expression is upregulated. At the same time, it increases the ribosomal levels and amino acid synthesis to react more effectively against adverse conditions. Under more extreme stress conditions, EHEC O157:H7 expressed genes related to an acidic environment (pH 4.5) upregulating the acid stress response pathways AR2-5, whereas, upon high concentrations of hydrogen peroxide, it transcribed higher levels of genes of the OxyR pathway and subsequently hydrogen peroxide oxidative stress-related genes.Competing Interest StatementThe authors have declared no competing interest.
ISSN:	2692-8205
DOI:	10.1101/2024.12.18.629128
Font:	Biological Science Database