Bacteria as Trigger for Chronic Gastrointestinal Disorders

Marteau, Philippe; Chaput, Ulriikka

doi:10.1159/000323879

Cited by 30 publications

(23 citation statements)

References 77 publications

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“…The GF animal model represents a fundamental tool to explore and elucidate the interaction between the host and its microbiota. In the absence of microbiota, GF animals are generally more susceptible to microbial infections (Fagundes et al, 2012); however, GF status can ensure a higher resistance to some other pathological conditions (generally involving inflammation), in which the indigenous microbiota acts as a trigger to induce the disease (Marteau & Chaput, 2011;Xavier & Podolsky, 2007). Fagundes et al (2012) demonstrated that GF mice did not survive a bacterial lung infection due to their inability to effectively process an appropriate inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of mucositis induced by irinotecan after microbial colonization in germ-free mice

et al. 2015

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Mucositis is one of the most debilitating side effects of chemotherapy and some previous studies suggest a role for indigenous microbiota in the course of this pathology. Therefore, the aim of our study was to evaluate the differences in phenotype between germ-free (GF) and conventional (CV) mice, and the role of b-glucuronidase-producing bacteria in the development of irinotecan treatment in a murine model. After mucositis induction, CV mice showed a significant increase in all inflammatory parameters when compared to GF mice. CV animals also showed more lesions of the intestinal epithelium, coherent with their higher intestinal permeability. The conventionalization of GF animals reversed their phenotype to that found in CV mice. In addition, gnotobiotic mice monoassociated with an Escherichia coli strain producing b-glucuronidase showed an increased permeability when compared to gnotobiotic mice monoassociated with an E. coli strain deleted for the gene encoding b-glucuronidase, but these did not show any differences in the influx of neutrophils, eosinophils or histological characteristics. Our data confirmed that components of the gut microbiota are involved in the signs of mucositis. Nevertheless, other mechanisms than this enzyme are involved in the irinotecan treatment, since the monoassociation was not able to restore the entire phenotype observed in the CV animals with irinotecan treatment in our murine model.

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Section: Discussionmentioning

confidence: 99%

Evaluation of mucositis induced by irinotecan after microbial colonization in germ-free mice

et al. 2015

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“…These pathogens are able to cause acute or chronic damage to the host (95,96) or are linked to (postinfectious) complications (97)(98)(99)(100)(101)(102)(103)(104)(105)(106)(107).…”

Section: Cas9 As a Regulator Of Bacterial Virulencementioning

confidence: 99%

The Role of CRISPR-Cas Systems in Virulence of Pathogenic Bacteria

Louwen

Staals

Endtz

et al. 2014

Microbiol Mol Biol Rev

216

178

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SUMMARY Clustered regularly interspaced short palindromic repeats (CRISPR) and CRISPR-associated (Cas) genes are present in many bacterial and archaeal genomes. Since the discovery of the typical CRISPR loci in the 1980s, well before their physiological role was revealed, their variable sequences have been used as a complementary typing tool in diagnostic, epidemiologic, and evolutionary analyses of prokaryotic strains. The discovery that CRISPR spacers are often identical to sequence fragments of mobile genetic elements was a major breakthrough that eventually led to the elucidation of CRISPR-Cas as an adaptive immunity system. Key elements of this unique prokaryotic defense system are small CRISPR RNAs that guide nucleases to complementary target nucleic acids of invading viruses and plasmids, generally followed by the degradation of the invader. In addition, several recent studies have pointed at direct links of CRISPR-Cas to regulation of a range of stress-related phenomena. An interesting example concerns a pathogenic bacterium that possesses a CRISPR-associated ribonucleoprotein complex that may play a dual role in defense and/or virulence. In this review, we describe recently reported cases of potential involvement of CRISPR-Cas systems in bacterial stress responses in general and bacterial virulence in particular.

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“…Diagnosis of a persistent infection can be difficult, as signs are not always obvious. A prolonged persistent infection can cause a chronic inflammatory state, which could lead to complications or even precipitation of certain diseases in susceptible hosts (2)(3)(4). It may also cause organ damage, which eventually weakens the immune system, leading to symptomatic infection.…”

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confidence: 99%

Colonization of Cecum Is Important for Development of Persistent Infection by Yersinia pseudotuberculosis

et al. 2014

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bYersiniosis is a human disease caused by the bacterium Yersinia pseudotuberculosis or Yersinia enterocolitica. The infection is usually resolved but can lead to postinfectious sequelae, including reactive arthritis and erythema nodosum. The commonly used Yersinia mouse infection model mimics acute infection in humans to some extent but leads to systemic infection and eventual death. Here, we analyzed sublethal infection doses of Y. pseudotuberculosis in mice in real time using bioluminescent imaging and found that infections using these lower doses result in extended periods of asymptomatic infections in a fraction of mice. In a search for the site for bacterial persistence, we found that the cecum was the primary colonization site and was the site where the organism resided during a 115-day infection period. Persistent infection was accompanied by sustained fecal shedding of cultivable bacteria. Cecal patches were identified as the primary site for cecal colonization during persistence. Y. pseudotuberculosis bacteria were present in inflammatory lesions, in localized foci, or as single cells and also in neutrophil exudates in the cecal lumen. The chronically colonized cecum may serve as a reservoir for dissemination of infection to extraintestinal sites, and a chronic inflammatory state may trigger the onset of postinfectious sequelae. This novel mouse model for bacterial persistence in cecum has potential as an investigative tool to unveil a deeper understanding of bacterial adaptation and host immune defense mechanisms during persistent infection.

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Bacteria as Trigger for Chronic Gastrointestinal Disorders

Cited by 30 publications

References 77 publications

Evaluation of mucositis induced by irinotecan after microbial colonization in germ-free mice

Evaluation of mucositis induced by irinotecan after microbial colonization in germ-free mice

The Role of CRISPR-Cas Systems in Virulence of Pathogenic Bacteria

Colonization of Cecum Is Important for Development of Persistent Infection by Yersinia pseudotuberculosis

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