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KMID : 0923620190190060038
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Immune Network
2019 Volume.19 No. 6 p.38 ~ p.38
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Human Immunity Against Campylobacter Infection
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Hameed Amber
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Abstract
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Campylobacter is a worldwide foodborne pathogen, associated with human gastroenteritis. The efficient translocation of Campylobacter and its ability to secrete toxins into host cells are the 2 key features of Campylobacter pathophysiology which trigger inflammation in intestinal cells and contribute to the development of gastrointestinal symptoms, particularly diarrhoea, in humans. The purpose of conducting this literature review is to summarise the current understanding of: i) the human immune responses involved in the elimination of Campylobacter infection and ii) the resistance potential in Campylobacter against these immune responses. This review has highlighted that the intestinal epithelial cells are the preliminary cells which sense Campylobacter cells by means of their cell-surface and cytosolic receptors, activate various receptors-dependent signalling pathways, and recruit the innate immune cells to the site of inflammation. The innate immune system, adaptive immune system, and networking between these systems play a crucial role in bacterial clearance. Different cellular constituents of Campylobacter, mainly cell membrane lipooligosaccharides, capsule, and toxins, provide protection to Campylobacter against the human immune system mediated killing. This review has also identified gaps in knowledge, which are related to the activation of following during Campylobacter infection: i) cathelicidins, bactericidal permeability-increasing proteins, chemokines, and inflammasomes in intestinal epithelial cells; ii) siglec-7 receptors in dendritic cell; iii) acute phase proteins in serum; and iv) T-cell subsets in lymphoid nodules. This review evaluates the existing literature to improve the understanding of human immunity against Campylobacter infection and identify some of the knowledge gaps for future research.
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KEYWORD
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Campylobacter, Lipooligosaccharides, Guillain-Barre Syndrome, Inflammasomes, Toll-like receptors, Antigen-presenting cells
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