The Helical Shape of Campylobacter jejuni Promotes In Vivo Pathogenesis by Aiding Transit through Intestinal Mucus and Colonization of Crypts.

Campylobacter jejuni is a helix-shaped enteric bacterial pathogen and a common cause of gastroenteritis. We recently developed a mouse model for this human pathogen utilizing the SIGIRR-deficient mouse strain, which exhibits significant intestinal inflammation in response to intestinal C. jejuni infection.

Insights into Campylobacter jejuni colonization of the mammalian intestinal tract using a novel mouse model of infection.

A lack of relevant disease models for Campylobacter jejuni has long been an obstacle to research into this common enteric pathogen. We recently published that mice deficient in Single IgG Interleukin-1 related receptor (SIGIRR), a repressor of MyD88-dependent innate immune signaling, were highly susceptible to enteric infection by murine bacterial pathogens. Subsequently, we successfully employed these mice as an animal model for the human pathogen C.

Microarray transposon tracking for the mapping of conditionally essential genes in Campylobacter jejuni.

Although whole genome approaches to the study of bacteria have grown substantially in the past decade, there is still a need for quick and easy methods for the determination of which genes are essential for the growth of these bacteria under specific growth conditions. There are numerous methods to accomplish this depending on the resources and equipment available, each with their own advantages and disadvantages. Here we describe a method we successfully employed to map the essential genes of Campylobacter jejuni using a microarray transposon tracking approach where we constructed a saturated transposon mutant library in the C.

A novel mouse model of Campylobacter jejuni gastroenteritis reveals key pro-inflammatory and tissue protective roles for Toll-like receptor signaling during infection.

Campylobacter jejuni is a major source of foodborne illness in the developed world, and a common cause of clinical gastroenteritis. Exactly how C. jejuni colonizes its host's intestines and causes disease is poorly understood.

Innate host responses to enteric bacterial pathogens: a balancing act between resistance and tolerance.

Infection by enteric bacterial pathogens activates pathogen recognition receptors, leading to innate responses that promote host defence. While responses that promote host 'resistance' to infection, through the release of antimicrobial mediators, or the recruitment of inflammatory cells aimed at clearing the infection are best known, recent studies have begun to identify additional innate driven responses that instead promote intestinal tissue repair and host survival. Described as infection 'tolerance' responses, we and others have primarily studied these responses in the Citrobacter rodentium infection model.