%0 Journal Article
%T Modification of Intestinal Microbiota and Its Consequences for Innate Immune Response in the Pathogenesis of Campylobacteriosis
%A Wycliffe Omurwa Masanta
%A Markus M. Heimesaat
%A Stefan Bereswill
%A Abdul Malik Tareen
%A Raimond Lugert
%A Uwe Gro£¿
%A Andreas E. Zautner
%J Journal of Immunology Research
%D 2013
%R 10.1155/2013/526860
%X Campylobacter jejuni is the leading cause of bacterial food-borne gastroenteritis in the world, and thus one of the most important public health concerns. The initial stage in its pathogenesis after ingestion is to overcome colonization resistance that is maintained by the human intestinal microbiota. But how it overcomes colonization resistance is unknown. Recently developed humanized gnotobiotic mouse models have provided deeper insights into this initial stage and host¡¯s immune response. These studies have found that a fat-rich diet modifies the composition of the conventional intestinal microbiota by increasing the Firmicutes and Proteobacteria loads while reducing the Actinobacteria and Bacteroidetes loads creating an imbalance that exposes the intestinal epithelial cells to adherence. Upon adherence, deoxycholic acid stimulates C. jejuni to synthesize Campylobacter invasion antigens, which invade the epithelial cells. In response, NF-¦ÊB triggers the maturation of dendritic cells. Chemokines produced by the activated dendritic cells initiate the clearance of C. jejuni cells by inducing the actions of neutrophils, B-lymphocytes, and various subsets of T-cells. This immune response causes inflammation. This review focuses on the progress that has been made on understanding the relationship between intestinal microbiota shift, establishment of C. jejuni infection, and consequent immune response. 1. Introduction Campylobacter jejuni is a Gram-negative, spiral-shaped, nonspore forming, and highly motile bacterium that grows optimally under microaerophilic conditions at 42¡ãC. The genome of C. jejuni is roughly 1.6 to 1.7£¿Mbp with a G+C ratio of approximately 31% [1]. C. jejuni has a wide spectrum of hosts ranging from wild birds, chicken, and turkey to mammals such as cattle, swine, sheep, and humans and can also be found in milk, meat, and stock water. C. jejuni is a highly prevalent commensal bacterium in all its hosts except for humans causing a bacterial food-borne illness known as campylobacteriosis. Campylobacteriosis has been found to be a usually self-limiting disease that is characterized by symptoms such as fever, abdominal cramps, bloody diarrhea, dizziness, and myalgia. However, in rare cases campylobacteriosis may lead to postinfectious complications like the Guillain-Barr¨¦ syndrome (including the most severe form: the Miller-Fisher syndrome), reactive arthritis (Reiter¡¯s syndrome), postinfectious irritable bowel syndrome, and potentially immunoproliferative small intestinal disease [2, 3]. Epidemiological studies have shown that the
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