MI004-04 Murine Models of Campylobacter jejuni Colonization and Enteritis - Completed
C. jejuni is a globally distributed human pathogen, a leading cause of food borne enteritis, and has been linked to chronic neurological and joint diseases. To combat this pathogen, it is important to develop murine models of enteritis induced by primary C. jejuni challenge employing mice with a genetic background and immune bias that enhances susceptibility. In 3 years, we will deliver: 1) an SOP for infection of IL-10 knockout mice with C. jejuni strains, and 2) reproducible mouse models for C. jejuni colonization, and C. jejuni enteritis.We propose 4 experiments. Exp#1: Genetic Background. We will test inbred IL-10 KO mice of different genetic backgrounds (e.g. C57BL/6, B6.129P2, NOD, C3H/HeJBir, C3Bir.129P2(B6)) for susceptibility to C. jejuni colonization and enteritis. Exp#2: Dose Response. We will determine the dose-response of C57BL/6 IL-10 -/- micegiven C. jejuni. Here, we will challenge groups of mice orally with C. jejuni 11168 in 10-fold dilutions and quantify colonization and enteritis levels using a C. jejuni specific RT-PCR assay to determine the optimal dilution for subsequent studies. Exp#3: Time Course. We will determine the time-course for colonization and enteritis to develop in C57BL/6 IL-10 -/- mice given C. jejuni. Here, groups of mice will be challenged with C. jejuni 11168 to quantify levels of colonization and enteritis over time. Exp#4: Mouse Adaptation. We will determine the effect of repeated mouse passage on the ability of C. jejuni to colonize the mouse GI tract and to cause enteritis. In all experiments, the two outcomes assessed will be colonization and enteritis (disease/pathology).
Publications:
Animal Modles of Campylobacter jejuni Infections
C57BL/6 and congenic interleukin-10 deficient mice can serve as
models of Campylobacter jejuni colonization and enteritis
C57BL/6 and Congenic Interleukin-10-Deficient Mice Can Serve as
Models of Campylobacter jejuni Colonization and Enteritis
C57BL/6 mice and their IL-10 knockout (KO) can serve as models of Campylobacter
jejuni colonization and enteritis
Campylobacter jejuni Infection Triggers Inflammatory Bowel Disease in IL-10 Knockout (KO) Mice of Various Genetic Backgrounds
Campylobacter jejuni-Induced Activation of Dendritic Cells Involves
Cooperative Signaling through Toll-Like Receptor 4
(TLR4)-MyD88 and TLR4-TRIF Axes
Dendritic cells from C57BL/6 mice undergo activation and induce
Th1-effector cell responses against Campylobacter jejuni
Genetic background of IL-10 -/- mice alters host–pathogen interactions with
Campylobacter jejuni and influences disease phenotype
IL-10 Knockout (KO) Mice of Various Genetic Backgrounds Develop nonprotective Isotype Specific Anti-Camplobacter jejuni IgG Antibiodies
Multiple factors interact to produce responses resembling
spectrum of human disease in Campylobacter jejuni infected
C57BL/6 IL-10-/- mice
Recombinant IL-4 Enhances Cam1 pylobacter jejuni Invasion of
2 Differentiated Monolayers of Intestinal Pig Epithelial Cells
Recombinant interleukin-4 enhances Campylobacter jejuni invasion of
intestinal pig epithelial cells (IPEC-1)
