Human Immunity AgainstCampylobacterInfection

Abstract

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 receptorsdependent 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.

Campylobacterinfections among Bulgarian children: molecular characterization and antimicrobial susceptibility

“…[1][2][3][4][5]. In addition to acute gastroenteritis, this pathogen has been associated with severe postinfectious complications such as Guillain-Barr e syndrome, Henoch-Schonlein purpura, and other autoimmune conditions [1,6]. In recent years, the incidence of campylobacteriosis has increased significantly, but it is still rarely reported officially in Bulgaria [7].…”

The Role of Immune Response and Microbiota on Campylobacteriosis

“…At the molecular level, the innate cells recognize the microbes of their microbialassociated molecular patterns (MAMPs), such as lipopolysaccharides (LPS) and flagellin. MAMP is a component of a microbe and is sensed by innate cellular pathogen recognition receptors (PRRs), such as toll-like receptors (TLRs), nucleotide oligomerization domain (NOD) like receptors (NLRs), and retinoic acid inducible gene-I (RIG-I) like receptors (RLRs) [26,27]. Previous articles have comprehensively reviewed the interaction between MAMP and PRR [28], hence we will not devote too much on them.…”

“…The Role of Immune Response and Microbiota on Campylobacteriosis DOI: http://dx.doi.org/10.5772/intechopen.96755 cells and macrophages to enhance immunity against the invading or intracellular microbes, while Th2 cells mediate class switching of B-cells to eliminate the extracellular microbes [38]. Besides Th1 and Th2 cells, Th17, Th22, and Treg may also be induced in campylobacteriosis as evidenced by the elevated cytokine markers of IL-17, IL-18, IL-22, IL-23, and IL-10 in patients' serum following infection with Campylobacter [26,46].…”

Work-related increases in titer of <i>Campylobacter jejuni</i> antibody among workers at a chicken processing plant in Miyazaki prefecture, Japan, independent of individual ingestion of edible raw chicken meat

“…In general, kinetics of humoral immunity of IgA after Campylobacter infection in humans increase in serum in the acute phase of infection (1-week post-infection) and rapidly decline to normal level after 14-20 days from the onset of symptoms [7,10]. In contrast, serum IgG antibodies are produced during convalescent phase of infection or antigen exposure ( 1week to 2 months), rising a few weeks after it begins, then decreasing and stabilizing for long period (1 year), and provide protection against subsequent Campylobacter infection [7].…”