Microbic Superinfection in Relapse of Inflammatory Bowel Disease

Weber, P; Koch, Matthias; Heizmann, W.; Scheurlen, Michael; Jenss, H; Hartmann, F

doi:10.1097/00004836-199206000-00008

Cited by 105 publications

(65 citation statements)

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“…C. jejuni was the initial focus of research (83)(84)(85), but it was not until 2009 that Gradel and colleagues provided evidence that indicated an association between C. jejuni infection and an increased risk of IBD (86). Furthermore, recent studies investigating the role of other emerging Campylobacter species in IBD have provided solid evidence that demonstrates an association between C. concisus and these gastrointestinal disorders (81,(87)(88)(89)(90)(91)(92)(93)(94).…”

Section: Inflammatory Bowel Diseasesmentioning

confidence: 99%

Global Epidemiology of Campylobacter Infection

et al. 2015

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SUMMARY Campylobacter jejuni infection is one of the most widespread infectious diseases of the last century. The incidence and prevalence of campylobacteriosis have increased in both developed and developing countries over the last 10 years. The dramatic increase in North America, Europe, and Australia is alarming, and data from parts of Africa, Asia, and the Middle East indicate that campylobacteriosis is endemic in these areas, especially in children. In addition to C. jejuni , there is increasing recognition of the clinical importance of emerging Campylobacter species, including Campylobacter concisus and Campylobacter ureolyticus . Poultry is a major reservoir and source of transmission of campylobacteriosis to humans. Other risk factors include consumption of animal products and water, contact with animals, and international travel. Strategic implementation of multifaceted biocontrol measures to reduce the transmission of this group of pathogens is paramount for public health. Overall, campylobacteriosis is still one of the most important infectious diseases that is likely to challenge global health in the years to come. This review provides a comprehensive overview of the global epidemiology, transmission, and clinical relevance of Campylobacter infection.

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Section: Inflammatory Bowel Diseasesmentioning

confidence: 99%

Global Epidemiology of Campylobacter Infection

et al. 2015

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“…There are also a few case reports of Campylobacter-associated hemolytic-uremic syndrome, which is a well-known sequela of infection with verocytotoxin (Shiga toxin)-producing Escherichia coli strains (151). Campylobacter strains have also been isolated from patients with inflammatory bowel disease (IBD) such as Crohn's disease and have been associated with flare-ups of IBD, although a causal link between the two is still under debate (21,67,178). A recent registry-based study in Denmark revealed very strong associations between Campylobacter infection and the development of IBD, but this association still needs to be confirmed (81).…”

Section: Sequelae Of Campylobacter Infectionmentioning

confidence: 99%

Host-Pathogen Interactions inCampylobacterInfections: the Host Perspective

et al. 2008

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SUMMARY Campylobacter is a major cause of acute bacterial diarrhea in humans worldwide. This study was aimed at summarizing the current understanding of host mechanisms involved in the defense against Campylobacter by evaluating data available from three sources: (i) epidemiological observations, (ii) observations of patients, and (iii) experimental observations including observations of animal models and human volunteer studies. Analysis of available data clearly indicates that an effective immune system is crucial for the host defense against Campylobacter infection. Innate, cell-mediated, and humoral immune responses are induced during Campylobacter infection, but the relative importance of these mechanisms in conferring protective immunity against reinfection is unclear. Frequent exposure to Campylobacter does lead to the induction of short-term protection against disease but most probably not against colonization. Recent progress in the development of more suitable animal models for studying Campylobacter infection has opened up possibilities to study the importance of innate and adaptive immunity during infection and in protection against reinfection. In addition, advances in genomics and proteomics technologies will enable more detailed molecular studies. Such studies combined with better integration of host and pathogen research driven by epidemiological findings may truly advance our understanding of Campylobacter infection in humans.

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“…While most cases are self-limiting, postinfection complications, including Guillain-Barré syndrome and irritable bowel syndrome, can arise (29,34). Campylobacter species are also commonly isolated from patients with colitis (28,55), and an acute enteric infection can induce the relapse of IBD (35,36,53). Moreover, several recent clinical studies indicate that an acute infection with Campylobacter is a risk factor for the subsequent development of IBD (12,13,51).…”

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confidence: 99%

Campylobacter jejuni Disrupts Protective Toll-Like Receptor 9 Signaling in Colonic Epithelial Cells and Increases the Severity of Dextran Sulfate Sodium-Induced Colitis in Mice

et al. 2012

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Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation associated with a dysregulated immune response to commensal bacteria in susceptible individuals. The relapse of IBD may occur following an infection with Campylobacter jejuni. Apical epithelial Toll-like receptor 9 (TLR9) activation by bacterial DNA is reported to maintain colonic homeostasis. We investigated whether a prior C. jejuni infection disrupts epithelial TLR9 signaling and increases the severity of disease in a model of mild dextran sulfate sodium (DSS) colitis in mice. In a further attempt to identify mechanisms, T84 monolayers were treated with C. jejuni followed by a TLR9 agonist. Transepithelial resistance (TER) and dextran flux across confluent monolayers were monitored. Immunohistochemistry, Western blotting, and flow cytometry were used to examine TLR9 expression. Mice colonized by C. jejuni lacked any detectable pathology; however, in response to low levels of DSS, mice previously exposed to C. jejuni exhibited significantly reduced weight gain and increased occult blood and histological damage scores. Infected mice treated with DSS also demonstrated a significant reduction in levels of the anti-inflammatory cytokine interleukin-25. In vitro studies indicated that apical application of a TLR9 agonist enhances intestinal epithelial barrier function and that this response is lost in C. jejuni-infected monolayers. Furthermore, infected cells secreted significantly more CXCL8 following the basolateral application of a TLR9 agonist. Surface TLR9 expression was reduced in C. jejuni-infected monolayers subsequently exposed to a TLR9 agonist. In conclusion, infection by C. jejuni disrupts TLR9-induced reinforcement of the intestinal epithelial barrier, and colonization by C. jejuni increases the severity of mild DSS colitis.

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Microbic Superinfection in Relapse of Inflammatory Bowel Disease

Cited by 105 publications

References 0 publications

Global Epidemiology of Campylobacter Infection

Global Epidemiology of Campylobacter Infection

Host-Pathogen Interactions inCampylobacterInfections: the Host Perspective

Campylobacter jejuni Disrupts Protective Toll-Like Receptor 9 Signaling in Colonic Epithelial Cells and Increases the Severity of Dextran Sulfate Sodium-Induced Colitis in Mice

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