Citrobacter rodentium (Cr) is a mouse pathogen that mimics many aspects of enteropathogenic Escherichia coli infections including producing attaching and effacing (A/E) lesions. Host-adapted (HA) Cr cells that are shed at the peak of infection have been reported to be hyper-infective. The exact mechanism underlying this phenomenon has remained elusive since the pathogen loses its HA 'status' immediately upon subculturing in laboratory media. We sequenced the entire transcriptome of Cr directly from the feces of infected mice and analyzed the gene expression pattern. We observed that the entire transcriptional machinery as well as several transcriptional regulators to be differentially expressed when compared with the transcriptome of cells grown on laboratory media. Major adhesion and effector genes, tir and eae, were highly expressed in HA along with many genes located on all five loci of enterocyte effacement regions (LEE 1-5). Notable absent among the HA expressed genes were 19 fimbrial operons and non-fimbrial adhesions and several non-LEE encoded effectors. These results demonstrate that host-adapted Cr has a unique transcriptome that is associated with increased host transmission.
Background: Enterohemorrhagic Escherichia coli (EHEC), a group of enteric pathogenic bacteria that is a major cause of human diarrheal disease, must interact with the diverse intestinal microbiome during colonization and subsequently overcome the environmental challenges to survive and cause disease. While this relationship, and how the microbiome modulates infection of EHEC, has been studied, it is less understood how the microbiome is impacted during treatment for an EHEC infection. One area that is notably lacking in knowledge is how vaccination can impact the intestinal microbiome composition, and therefore, influence vaccine efficacy.
Enteropathogenic (EPEC) is a bacterium that causes attaching/effacing (A/E) lesions and serious diarrheal disease, a major health issue in developing countries. EPEC pathogenicity results from the effect of virulence factors and dysregulation of host responses. Polyamines, including spermidine, play a major role in intestinal homeostasis.
Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, 107D Animal, Veterinary and Biomedical Sciences Building, University Park, PA 16801, USA. Electronic address:
Reactive oxygen species (ROS) play a critical role in modulating a range of proinflammatory functions in neutrophils, as well as regulating neutrophil apoptosis and facilitating the resolution of an inflammatory response. Selenoproteins with the 21st amino acid, selenocysteine (Sec), regulate immune mechanisms through the modulation of redox homeostasis aiding in the efficient resolution of inflammation, while their role in neutrophil functions during diseases remains unclear. To study the role of selenoproteins in neutrophils during infection, we challenged the granulocyte-specific tRNA (Trsp) knockout mice (Trsp) with Citrobacter rodentium (C.
Background: Enterohemorrhagic (EHEC), a group of enteric pathogenic bacteria that is a major cause of human diarrheal disease, must interact with the diverse intestinal microbiome during colonization and subsequently overcome the environmental challenges to survive and cause disease. While this relationship, and how the microbiome modulates infection of EHEC, has been studied, it is less understood how the microbiome is impacted during treatment for an EHEC infection. One area that is notably lacking in knowledge is how vaccination can impact the intestinal microbiome composition, and therefore, influence vaccine efficacy.
Department of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, United States of America.
Attaching and effacing (A/E) bacterial pathogens consist of human pathogens enteropathogenic Escherichia coli, enterohemorrhagic E. coli and their murine equivalent Citrobacter rodentium (CR). Emerging evidence suggests that the complex pathogen-microbiota-host interactions are critical in conferring A/E pathogen infection-induced severe symptoms and lethality in immunocompromised hosts; however, the precise underlying mechanisms remain enigmatic.
