Article
Utility of the Citrobacter rodentium infection model in laboratory mice.
Division of Comparative Medicine, Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
Current opinion in gastroenterology (impact factor:
4.33).
02/2008;
24(1):32-7.
DOI:10.1097/MOG.0b013e3282f2b0fb
Source: PubMed
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Citations (0)
- Cited In (20)
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Article: CX(3)CR1(+) macrophages support IL-22 production by innate lymphoid cells during infection with Citrobacter rodentium.
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ABSTRACT: Innate immune cells, such as intestinal epithelial cells, dendritic cells (DCs), macrophages, granulocytes, and innate lymphoid cells provide a first line of defence to enteric pathogens. To study the role of CX(3)CR1(+) DCs and macrophages in host defence, we infected CX(3)CR1-GFP animals with Citrobacter rodentium. When transgenic CX(3)CR1-GFP animals are infected with the natural mouse pathogen C. rodentium, CX(3)CR1(-/-) animals showed a delayed clearance of C. rodentium as compared with (age- and sex-matched) wild-type B6 animals. The delayed clearance of C. rodentium is associated with reduced interleukin (IL)-22 expression. In C. rodentium-infected CX(3)CR1-GFP animals, IL-22 producing lymphoid-tissue inducer cells (LTi cells) were selectively reduced in the absence of CX(3)CR1. The reduced IL-22 expression correlates with decreased expression of the antimicrobial peptides RegIIIβ and RegIIIγ. The depletion of CX(3)CR1(+) cells by diphtheria toxin injection in CX(3)CR1-GFP × CD11c.DOG animals confirmed the role of CX(3)CR1(+) phagocytes in establishing IL-22 production, supporting the clearance of a C. rodentium infection.Mucosal Immunology advance online publication 1 August 2012. doi:10.1038/mi.2012.61.Mucosal Immunology 08/2012; · 6.96 Impact Factor -
Article: Chromosomal complementation using Tn7 transposon vectors in Enterobacteriaceae.
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ABSTRACT: Genetic complementation in many bacteria is commonly achieved by reintroducing functional copies of the mutated or deleted genes on a recombinant plasmid. Chromosomal integration systems using the Tn7 transposon have the advantage of providing a stable single-copy integration that does not require selective pressure. Previous Tn7 systems have been developed, although none have been shown to work effectively in a variety of enterobacteria. We have developed several mini-Tn7 and transposase vectors to provide a more versatile system. Transposition of Tn7 at the chromosomal attTn7 site was achieved by a classical conjugation approach, wherein the donor strain harbored the mini-Tn7 vector and the recipient strain possessed the transposase vector. This approach was efficient for five different pathogenic enterobacterial species. Thus, this system provides a useful tool for single-copy complementation at an episomal site for research in bacterial genetics and microbial pathogenesis. Furthermore, these vectors could also be used for the introduction of foreign genes for use in biotechnology applications, vaccine development, or gene expression and gene fusion constructs.Applied and environmental microbiology 06/2012; 78(17):6001-8. · 3.69 Impact Factor -
Article: A novel murine infection model for Shiga toxin-producing Escherichia coli.
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ABSTRACT: Enterohemorrhagic E. coli (EHEC) is an important subset of Shiga toxin-producing (Stx-producing) E. coli (STEC), pathogens that have been implicated in outbreaks of food-borne illness and can cause intestinal and systemic disease, including severe renal damage. Upon attachment to intestinal epithelium, EHEC generates "attaching and effacing" (AE) lesions characterized by intimate attachment and actin rearrangement upon host cell binding. Stx produced in the gut transverses the intestinal epithelium, causing vascular damage that leads to systemic disease. Models of EHEC infection in conventional mice do not manifest key features of disease, such as AE lesions, intestinal damage, and systemic illness. In order to develop an infection model that better reflects the pathogenesis of this subset of STEC, we constructed an Stx-producing strain of Citrobacter rodentium, a murine AE pathogen that otherwise lacks Stx. Mice infected with Stx-producing C. rodentium developed AE lesions on the intestinal epithelium and Stx-dependent intestinal inflammatory damage. Further, the mice experienced lethal infection characterized by histopathological and functional kidney damage. The development of a murine model that encompasses AE lesion formation and Stx-mediated tissue damage will provide a new platform upon which to identify EHEC alterations of host epithelium that contribute to systemic disease.The Journal of clinical investigation 10/2012; · 15.39 Impact Factor
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Keywords
acute diarrheal illness
adaptive immune responses
bacterial virulence determinants
C. rodentium
C. rodentium infection
diarrhea-causing pathogens
disease ranges
enterohemorrhagic E. coli infection
enteropathogenic Escherichia coli
epithelial hyperplasia
fatal infection
growing number
health status
inbred strains
infecting laboratory mice
murine bacterial pathogen Citrobacter rodentium
relevant in-vivo model system
subclinical epithelial hyperplasia
therapeutic agents
useful in-vivo model