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Immunity And Disease: Campylobacter Jejuni Infections

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Immunity And Disease: Campylobacter Jejuni Infections Question: Discuss about the Immunity and Disease for Campylobacter Jejuni Infections.   Answer: Campylobacter jejuni is a zoonotic pathogenic bacterium that is a causative organism for gastroenteritis in humans which is called campylobacteriosis. Infections caused by Campylobacter are more common than those caused by other pathogens, such as Salmonella, Shigella or Escherichia coli O157:H7. Consumption of undercooked poultry and handling of uncooked chicken causes most of the infections. Although the organism does not cause infection in chicken, it inhabits the intestine (Wigley, 2013). Contaminated drinking water and raw milk from infected cattle could also cause infection (Humphrey, 1987). Chopping of vegetables on surfaces contaminated by poultry can increase the risk of food borne infection if the vegetables are served raw or partially cooked. Symptoms of an infection include fever, abdominal cramps and diarrhoea and diagnosis is usually done by culturing stool samples of patients. Presence of mucus and blood in the stools is common. Antibiotic resistant Campylobacter strains are difficult to treat (Acheson & Allos, 2001). The infection by Campylobacter jejuni causes inflammation of the intestinal surfaces and this leads to malabsorption of nutrients. C. jejuni is also known to cause autoimmune disorders Guillain-Barre syndrome and the Miller-Fisher syndrome.   Other than gastroenteritis, the organism is associated with inflammatory bowel syndrome, colon cancer and Barrett’s oesophagus. Other than the gastrointestinal system, it can cause infections in the lung, the pathogen has been known to cause brain abscess, bacteremia, meningitis and arthritis (Kaakoush, et al., 2015). The infection is known to occur more commonly in infants and children blow the age of five years and among young adults. A higher number of cases has been reported from North America, Australia and Europe. The problem of gastroenteritis is common in the developing countries. When infection by Campylobacter jejuni occurs, the immune system is able to recognize the pathogen as non-self and launches an immune response against the organism. The human innate has evolved in such a manner that it can recognize invading pathogens. It has to overcome the stealth mechanisms that the pathogen in capable of when it evades detection by the host’s immune system  The sentinel cells of the mucosal epithelium of the intestine are able to recognize bacteria by their pattern recognition receptors (PRRs). The bile acids that include the cholates and the deoxycholates have a detergent like action and can kill bacteria. In the human intestine the concentration of the bile acids ranges from 0.2%-2% (Fonseca, et al., 2016). Another level of protection from infection is provided by the mucus gel layer that coats the intestinal epidermis. It is made up of the mucin proteins or the MUCs (Hollingsworth & Swanson, 2004). The MUCs play an important role in immune surveillance.  The mucins associated with the membrane, example, MUC1 and the secreted mucins MUC2 re proteins with domains that are arrays of tandem repeats and re rich in the amino acids threonine, serine and proline, the PTS domains. These domains are glycosylated. It has been found that inappropriate expression of MUC1 can predispose human beings to inflammatory and infectious diseases (Sheng, et al., 2013). MUC1 is overexpressed in case of C. jejuni infection of the intestine. It promotes anti-inflammatory effect against the bacteria by reducing the activation of NF-κB and decrease in IL-8 cytokine production (Fonseca, et al., 2016).   When MUC1 expression is less the surface expression on antigen presenting cells (APCs) of CD40, CD80 and CD86 increases. This results in a higher secretion of TNF-α and a greater stimulation of CD4+ T cells results. Lack of MUC2 causes increase in the production of pro-inflammatory cytokines occurs, these include, IL-1β, TNF-α and INF-γ. Local inflammation protects against C. jejuni infection (Fonseca, et al., 2016). The adaptive immune response against Campylobacter jejuni is multipronged. Phagocytosis is preceded by the recognition of bacterial antigens through the pattern recognition receptors. The processing of antigens occurs via the lysosomal pathway, where the lysosomal enzymes degrade antigens. The Major Histocompatibity Complex presents the epitopes and epitope recognition occurs through the t cell receptors on CD4+ while the MHC is recognised by the CD8+. Recognition of the soluble antigens when present is mediated by the B cell receptors. The secretion of the antibody isotypes follows and complement activation by antibodies also occurs. The opsonization of the bacteria by antibodies is followed by phagocytosis. Interferon-gamma activates the macrophages and lymphocytes. The antigen presenting cells produce the cytokine IL-12 which in turn induces interferon-gamma by the T helper cells. Among the strategies that Campylobacter jejuni uses to evade the killing effect of the immune response is the presence of a lipopolysaccharide capsule, which is not a regular feature of other enteric pathogens. The capsule helps to evade the non-specific action of lysozyme, complement, phagocytes and other constituents of the serum through which the serum can kill the bacteria. Specific components of the serum that include antibodies and lymphocytes can also lyse or kill or inhibit the growth of pathogenic bacteria once contact is made with the pathogen. The presence of the LPS capsule also facilitates the colonization of C. jejuni in the mouse intestine (Mauea, et al., 2013). The epithelial cells separate the interstitium of the body from the lumen of the intestine. The paracellular spaces remain sealed by the tight junctions that consist of occludins and claudins, the transmembrane proteins. Even a minor change n the structure of the occludins facilitates the entry of C. jejuni to the inner reaches and cause infection (Clayburgh, et al., 2004).   Interleukins IL-23p19, IL-22 and IL-18 have important functions in conferring the host with immunity. It has been found in the murine model that upon C. jejuni infection, there is an upregulation of these interleukins. In the intestine the IL-23 is understood to play the role of a master regulator in the development of a mucosal immune response in the event of intestinal infection that is followed by inflammation. IL-22 is part of the IL-10 family of interleukins and it exerts a three pronged effect, it has potent anti-microbial activity, is tissue-protective and has inflammatory properties. In the large intestine, the IL-22 exhibits anti-inflammatory properties, while in the small intestine it acts a pro-inflammatory cytokine. In a study on the impact of the IL-23, IL-22 and IL-18 axis upon C. jejuni infection, it was seen that IL-18 mediates intestinal and systemic immune responses (Bereswill, et al., 2016). Due to the intestinal immune response there is production of  IL 17 by the CD4+ cells in the intestine. The production of this interleukin has been shown to reduce the colonisation of the intestine by C. jejuni. But the absence of the capsule in mutant C. jejuni makes the action of the IL 17 more potent and the size of the colony is reduced. The T helper 17 response has an important role in maintaining gut homeostasis besides initiating  protective immune response against intestinal pathogens (Mauea, et al., 2013). The Th17 mediates the response to pathogens through innate immunity, which is non-specific and not in response to a particular antigen and through adaptive immunity which includes the B-cell mediated antibody response and the cell mediated response that is due to the function of the T lymphocytes. The innate Th17 response is due to the filamentous bacteria that colonize the gut and are a part of the symbiotic gut microbiota. The innate Th17 response occurs quickly under the effect of the cytokines, but the adaptive response may take a few days to a few weeks to take effect. IL-17 and IL-22 are the cytokines that bring on the quick innate response and are in turn expressed due to the upstream cytokines IL-1, IL-6 and IL-23. IL-17 is known to bring about induction of inflammation and through recruitment of neutrophils to the site of infection in the intestine. Whereas, IL-22 induces cells of the intestinal epithelium to produce antibacterial molecules. In a study on the cells cultured from a colon biopsy, cocultured with C. jejuni that was treated to IL-17, it was found that the ability of the pathogen to invade the epithelial cells was reduced (Edwards LA, et al., 2010). The cytokine production is downregulated when pathogenic strains are devoid of their usual capsules. Probably the capsules play a role in eliciting a stronger innate immune response. The Toll-like receptor 4 is a transmembrane receptor that belongs to the pattern recognition receptor family. In response to recognition of molecular patterns on the capsules of pathogenic bacteria it activates the innate immune response through the NF-κB signalling and stimulates the release of cytokines that induce inflammation (Molteni, et al., 2016). The Toll-like receptor 4 is a mediator of the pro-inflammatory response. It has been shown to be active against the capsular lipopolysaccharide of the C. jejuni. The capsule also resists the action of the complement system and prevents puncturing of the cell wall (Mauea, et al., 2013).   The MeOPN or the O-methyl phosphoramidate capsule modification in the C. jejuni capsule is present in most pathogenic strains of the bacterium.A mutant which lacked MeOPN in its capsule was susceptible to killing by the complement system and human serum (van Alphen, et al., 2014). These and other features that are characteristic of the surface of the pathogen help it to circumvent and evade the immune response of the human body and in particular the intestinal micro – environment, colonize and infect the human intestine. The role of C. jejuni in development of autoimmune disorders has also been investigated. This organism is known to produce glycoconjugates. These include the human ganglioside kind of determinants and activators of the TLRs (the Toll-like receptors). Autoimmune induction is preceded by IL-1β secretion that is dependent on inflammasome or the MyD88-mediated TLR activation. C. jejuni does target MyD88, NLRP3 inflammasome, sialic-acid binding immunoglobulin like lectins (Siglecs) and the macrophage galactose type lectin besides the immunoglobulin like receptors, the TREM2 and the LMIR5CD300b. TIR-domain containing adaptor inducing interferon-β or the TRIF is known to mediate the type I interferon production that triggers the humoral immune response and the class switching of immunoglobulins. Upon activation the Siglec-1 activates the inflammatory response and phagocytosis. TREM2 also plays a role in phagocytosis. When autoreactive lymphocytes are present and C. jejuni activates the innate immune response, autoimmune diseases may be triggered (Phonqsisay, 2016). In conclusion, the pathogenic bacterium Campylobacter jejuni is a foodborne pathogen that infects the intestinal wall and can cause symptoms such as, fever, diarrhoea and there could be traces of blood or mucus in the stools. The foods that can cause infection are improperly cooked poultry, raw milk and handling of raw meat. The organism is microaerophilic and it can infect the intestinal wall. The human body’s immune system can identify and kill the infectious pathogen. Both innate and adaptive immunity play a role in eliminating the pathogen. But Campylobacter jejuni can evade the immune response using a host of mechanisms. Principal among the evasive tools that it employs is the presence of the lipopolysaccharide capsule. Autoimmune disorders such as Guillain-Barre syndrome and the Miller-Fisher syndrome can occur weeks after the symptoms of the infection have subsided.   References Acheson, D. & Allos, B., 2001. Campylobacter jejuni Infections: Update on Emerging Issues and Trends. Clinical Infectious Diseases, 32(8), pp. 1201-1206. Bereswill, S. et al., 2016. Interleukin-18 Mediates Immune Responses to Campylobacter jejuni Infection in Gnotobiotic Mice. PLoS ONE, 11(6), p. e0158020. Clayburgh, D., Shen, L. & Turner, J., 2004. A porous defense: the leaky epithelial barrier in intestinal disease.. Laboratory investigation , 84(3), pp. 282-91.. Edwards LA, N. K. M. D. S. H. Z. M. W. B. D. N. L. K., Wedderburn, L. & Bajaj-Elliott, M., 2010. 2010. Delineation of the innate and adaptive T-cell immune outcome in the human host in response to Campylobacter jejuni infection.. PLoS ONE, Volume 5, p. e15398.. Fonseca, B., Fernandez, H. & Rossi, D., 2016. Campylobacter spp. and Related Organisms in Poultry: Pathogen-Host Interactions, Diagnosis and Epidemiology. s.l.:Springer. Hollingsworth, M. & Swanson, B., 2004. Mucins in cancer: protection and control of the cell surface. Nature Reviews Cancer, Volume 4, pp. 45-60. Humphrey, T., 1987. Campylobacterjejuni in dairy cows and raw milk. Epidemiology and infection, Volume 98, pp. 263-269. Kaakoush, N. O., Castaño-Rodríguez, N., Mitchell, H. M. & Man, S. M., 2015. Global Epidemiology of Campylobacter Infection.. Clinical Microbiology Reviews, 28 (3), p. 687–720. Mauea, A. et al., 2013. The Polysaccharide Capsule of Campylobacter jejuni Modulates the Host Immune Response. Infection and Immunity, 81(3), pp. 665-672. Molteni, M., Gemma, S. & Rossetti, C., 2016. The Role of Toll-Like Receptor 4 in Infectious and Noninfectious Inflammation. Mediators of Inflammation, p. 6978936. Phonqsisay, V., 2016. The immunobiology of Campylobacter jejuni: Innate immunity and autoimmune diseases.. Immunobiology, 221(4), pp. 535-43. Sheng, Y. et al., 2013. MUC1 and MUC13 differentially regulate epithelial inflammation in response to inflammatory and infectious stimuli.. Mucosal Immunology, 6(3), pp. 557-68. van Alphen, L. et al., 2014. Biological roles of the O-methyl phosphoramidate capsule modification in Campylobacter jejuni.. PLoS ONE, 9(1), p. e87051. Wigley, P., 2013. Immunity to bacterial infection in the chicken.. Developmental and comparative immunology, 41(3), pp. 413-7. .

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