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1.
PLoS One ; 9(2): e88043, 2014.
Article in English | MEDLINE | ID: mdl-24558375

ABSTRACT

Campylobacter jejuni is an important cause of bacterial diarrhea worldwide. The pathogenesis of C. jejuni is poorly understood and complicated by phase variation of multiple surface structures including lipooligosaccharide, capsule, and flagellum. When C. jejuni strain 81-176 was plated on blood agar for single colonies, the presence of translucent, non-motile colonial variants was noted among the majority of opaque, motile colonies. High-throughput genomic sequencing of two flagellated translucent and two opaque variants as well as the parent strain revealed multiple genetic changes compared to the published genome. However, the only mutated open reading frame common between the two translucent variants and absent from the opaque variants and the parent was motA, encoding a flagellar motor protein. A total of 18 spontaneous motA mutations were found that mapped to four distinct sites in the gene, with only one class of mutation present in a phase variable region. This study exemplifies the mutative/adaptive properties of C. jejuni and demonstrates additional variability in C. jejuni beyond phase variation.


Subject(s)
Bacterial Proteins/genetics , Campylobacter jejuni/genetics , Mutation , Amino Acid Sequence , Base Sequence , Escherichia coli/genetics , Genetic Variation , Genome, Bacterial , Molecular Sequence Data , Open Reading Frames , Phenotype , Sequence Homology, Amino Acid
2.
Infect Immun ; 81(3): 665-72, 2013 Mar.
Article in English | MEDLINE | ID: mdl-23250948

ABSTRACT

Campylobacter jejuni is a major cause of bacterial diarrheal disease worldwide. The organism is characterized by a diversity of polysaccharide structures, including a polysaccharide capsule. Most C. jejuni capsules are known to be decorated nonstoichiometrically with methyl phosphoramidate (MeOPN). The capsule of C. jejuni 81-176 has been shown to be required for serum resistance, but here we show that an encapsulated mutant lacking the MeOPN modification, an mpnC mutant, was equally as sensitive to serum killing as the nonencapsulated mutant. A nonencapsulated mutant, a kpsM mutant, exhibited significantly reduced colonization compared to that of wild-type 81-176 in a mouse intestinal colonization model, and the mpnC mutant showed an intermediate level of colonization. Both mutants were associated with higher levels of interleukin 17 (IL-17) expression from lamina propria CD4(+) cells than from cells from animals infected with 81-176. In addition, reduced levels of Toll-like receptor 4 (TLR4) and TLR2 activation were observed following in vitro stimulation of human reporter cell lines with the kpsM and mpnC mutants compared to those with wild-type 81-176. The data suggest that the capsule polysaccharide of C. jejuni and the MeOPN modification modulate the host immune response.


Subject(s)
Campylobacter Infections/microbiology , Campylobacter jejuni/physiology , Polysaccharides, Bacterial/physiology , Animals , Cytokines/genetics , Cytokines/metabolism , Gene Expression Regulation/immunology , HEK293 Cells , Humans , Mice , Mutation , NF-kappa B/genetics , NF-kappa B/metabolism , Signal Transduction , Toll-Like Receptors/genetics , Toll-Like Receptors/metabolism
3.
J Biomed Biotechnol ; 2011: 258185, 2011.
Article in English | MEDLINE | ID: mdl-21274267

ABSTRACT

Escherichia coli O157:H7 has been responsible for multiple food- and waterborne outbreaks of diarrhea and/or hemorrhagic colitis (HC) worldwide. More importantly, a portion of E. coli O157:H7-infected individuals, particularly young children, develop a life-threatening sequela of infection called hemolytic uremic syndrome (HUS). Shiga toxin (Stx), a potent cytotoxin, is the major virulence factor linked to the presentation of both HC and HUS. Currently, treatment of E. coli O157:H7 and other Stx-producing E. coli (STEC) infections is limited to supportive care. To facilitate development of therapeutic strategies and vaccines for humans against these agents, animal models that mimic one or more aspect of STEC infection and disease are needed. In this paper, we focus on the characteristics of various mouse models that have been developed and that can be used to monitor STEC colonization, disease, pathology, or combinations of these features as well as the impact of Stx alone.


Subject(s)
Disease Models, Animal , Escherichia coli Infections/microbiology , Escherichia coli Infections/pathology , Escherichia coli O157 , Shiga Toxins , Animals , Humans , Mice
4.
Vaccine ; 28(30): 4777-85, 2010 Jul 05.
Article in English | MEDLINE | ID: mdl-20472033

ABSTRACT

Previously, we showed that the Shiga toxin type 2 (Stx2)-expressing Escherichia coli O157:H7 strain 86-24 colonized mice better than did its isogenic stx(2) negative mutant. Here, we confirmed that finding by demonstrating that Stx2 given orally to mice increased the levels of the 86-24 stx(2) mutant shed in feces. Then we assessed the impact of Stx2-neutralizing antibodies, administered passively or generated by immunization with an Stx2 toxoid, on E. coli O157:H7 colonization of mice. We found that such antibodies reduced the E. coli O157:H7 burden in infected mice and, as anticipated, also protected them from weight loss and death.


Subject(s)
Antibodies, Bacterial/immunology , Antibodies, Neutralizing/immunology , Escherichia coli Infections/microbiology , Escherichia coli Infections/prevention & control , Escherichia coli O157/genetics , Escherichia coli O157/immunology , Shiga Toxin 2/immunology , Animals , Enzyme-Linked Immunosorbent Assay , Escherichia coli Infections/immunology , Feces/chemistry , Female , Immunization, Passive , Mice , Mice, Inbred BALB C , Neutralization Tests , Rabbits , Shiga Toxin 2/genetics , Toxoids/immunology , Toxoids/therapeutic use , Vaccination , Weight Loss
5.
Microb Pathog ; 48(3-4): 131-42, 2010.
Article in English | MEDLINE | ID: mdl-20096770

ABSTRACT

Escherichia coli O157:H7 is a food-borne pathogen that can cause hemorrhagic colitis and, occasionally, hemolytic uremic syndrome, a sequela of infection that can result in renal failure and death. Here we sought to model the pathogenesis of orally-administered E. coli O157:H7 in BALB/c mice with an intact intestinal flora. First, we defined the optimal dose that permitted sustained fecal shedding of E. coli O157:H7 over 7 days ( approximately 10(9) colony forming units). Next, we monitored the load of E. coli O157:H7 in intestinal sections over time and observed that the cecum was consistently the tissue with the highest E. coli O157:H7 recovery. We then followed the expression of two key E. coli O157:H7 virulence factors, the adhesin intimin and Shiga toxin type 2, and detected both proteins early in infection when bacterial burdens were highest. Additionally, we noted that during infection, animals lost weight and approximately 30% died. Moribund animals also exhibited elevated levels of blood urea nitrogen, and, on necropsy, showed evidence of renal tubular damage. We conclude that conventional mice inoculated orally with high doses of E. coli O157:H7 can be used to model both intestinal colonization and subsequent development of certain extraintestinal manifestations of E. coli O157:H7 disease.


Subject(s)
Disease Models, Animal , Escherichia coli Infections/microbiology , Escherichia coli Infections/pathology , Adhesins, Bacterial/biosynthesis , Animals , Body Weight , Escherichia coli Proteins/biosynthesis , Feces/microbiology , Female , Gastrointestinal Tract/microbiology , Gene Expression Profiling , Humans , Kidney Tubules/pathology , Mice , Mice, Inbred BALB C , Shiga Toxin 2/biosynthesis , Survival Analysis , Urea/blood , Virulence Factors/biosynthesis
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