A Potential Role of Salmonella Infection in the Onset of Inflammatory Bowel Diseases

Schultz, Bárbara M.; Paduro, Carolina A.; Salazar, Geraldyne A.; Salazar-Echegarai, Francisco J.; Sebastián, Valentina P.; Riedel, Claudia A.; Kalergis, Alexis M.; Álvarez-Lobos, Manuel; Bueno, Susan M.

doi:10.3389/fimmu.2017.00191

Cited by 74 publications

(60 citation statements)

References 137 publications

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“…Several viral pathogens have been associated with IBD (38)(39)(40)(41). Similarly, a number of bacterial pathogens, such as Salmonella and Campylobacter, have been linked to IBD (42)(43)(44). For example, adherent invasive Escherichia coli is commonly found in Crohn's disease patients with ileal involvement (45), whereas Yersinia enterocolitica has been associated with ulcerative colitis in adults (46).…”

Section: Discussionmentioning

confidence: 99%

GiardiaInfection of the Small Intestine Induces Chronic Colitis in Genetically Susceptible Hosts

Dann

Hanson

et al. 2018

The Journal of Immunology

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The lumen-dwelling protozoan is an important parasitic cause of diarrheal disease worldwide. Infection can persist over extended periods with minimal intestinal inflammation, suggesting that may attenuate host responses to ensure its survival, although clearance eventually occurs in most cases. IL-10 is an anti-inflammatory regulator critical for intestinal homeostasis and controlling host responses to bacterial exposure, yet its potential role in coordinating antiprotozoal host defense in the intestine is not known. In this study, we found that murine infection with the natural enteric pathogen induced a transient IL-10 response after 2-4 wk at the primary site of infection in the upper small intestine, but parasite colonization and eradication were not affected by the absence of the cytokine in gene-targeted mice. However, IL-10 was critical for controlling infection-associated immunological sequelae in the colon because severe and persistent diarrhea and colitis were observed in IL-10-deficient mice within 1-2 wk postinfection but not in uninfected littermate controls. Inflammation was characterized by epithelial hyperplasia, neutrophil and macrophage expansion, and Th1 induction and could be prevented by blockade of IL-12/IL-23 p40 but not depletion of CD11c dendritic cells. Furthermore, the intestinal microbiota underwent characteristic shifts in composition and was required for disease because antibiotics and loss of TLR signaling in MyD88-deficient mice protected against colitis. Together, our data suggest that transient infection by a luminal and seemingly noninflammatory pathogen can trigger sustained colitis in genetically susceptible hosts, which has broader implications for understanding postinfectious syndromes and other chronic intestinal inflammatory conditions.

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Section: Discussionmentioning

confidence: 99%

GiardiaInfection of the Small Intestine Induces Chronic Colitis in Genetically Susceptible Hosts

Dann

Hanson

et al. 2018

The Journal of Immunology

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“…Mesalazine inhibits the growth of Mycobacterium avium subspecies paratuberculosis, which has been reported to be intimately linked to the etiology of CD [76], in a dose-dependent manner in vitro [77]. Another study has reported that mesalazine downregulates the gene expression that is associated with bacterial invasiveness and antibiotic resistance in Salmonella enterica serovar Typhimurium [78], which could promote the onset of IBD after its infection [79,80]. Furthermore, mesalazine inhibits the growth of sulfate-reducing bacteria and suppresses sulfide production in IBD patients [81,82].…”

Section: The Effects Of Medication For Ibd On Gut Microbiotamentioning

confidence: 99%

Gut microbiota in the pathogenesis of inflammatory bowel disease

Nishida

Inoüe

Inatomi

et al. 2017

Clin J Gastroenterol

1,016

709

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Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, is a chronic and relapsing inflammatory disorder of the intestine. Although its incidence is increasing globally, the precise etiology remains unclear and a cure for IBD has yet to be discovered. The most accepted hypothesis of IBD pathogenesis is that complex interactions between genetics, environmental factors, and the host immune system lead to aberrant immune responses and chronic intestinal inflammation. The human gut harbors a complex and abundant aggregation of microbes, collectively referred to as the gut microbiota. The gut microbiota has physiological functions associated with nutrition, the immune system, and defense of the host. Recent advances in next-generation sequencing technology have identified alteration of the composition and function of the gut microbiota, which is referred to as dysbiosis, in IBD. Clinical and experimental data suggest dysbiosis may play a pivotal role in the pathogenesis of IBD. This review is focused on the physiological function of the gut microbiota and the association between the gut microbiota and pathogenesis in IBD. In addition, we review the therapeutic options for manipulating the altered gut microbiota, such as probiotics and fecal microbiota transplantation.

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“…In patients with IBD, the abundance of intestinal symbiotic microbiota decreased, and that deficiency led to decreased secretion of antimicrobial peptides (α‐defensins) from Paneth and Goblet cells and increased REGIIIγ (Schultz et al . 2017). Notably, IBD patients showed a reduction of some Firmicutes ( Faecalibacterium prausnitzii ; a butyrate‐producer), Verrucomicrobia ( Akkermansia muciniphila ; a propionate‐producer) and an increase of Proteobacteria (Mahalhal et al .…”

Section: Intestinal Diseasesmentioning

confidence: 99%

“…Activated macrophages produce pro‐inflammatory cytokines that overstimulate Th1 or Th17 cells, to induce inflammation (Schultz et al . 2017). The loss of intestinal barrier integrity leads to increased bacterial antigen translocation and stimulation of the inflammatory response of intestinal mucosa, which is the core pathological feature of IBD.…”

Section: Intestinal Diseasesmentioning

confidence: 99%

Gut dysbacteriosis and intestinal disease: mechanism and treatment

Meng

Zhang

Cao³

et al. 2020

J. Appl. Microbiol.

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Summary The gut microbiome functions like an endocrine organ, generating bioactive metabolites, enzymes or small molecules that can impact host physiology. Gut dysbacteriosis is associated with many intestinal diseases including (but not limited to) inflammatory bowel disease, primary sclerosing cholangitis‐IBD, irritable bowel syndrome, chronic constipation, osmotic diarrhoea and colorectal cancer. The potential pathogenic mechanism of gut dysbacteriosis associated with intestinal diseases includes the alteration of composition of gut microbiota as well as the gut microbiota–derived signalling molecules. The many correlations between the latter and the susceptibility for intestinal diseases has placed a spotlight on the gut microbiome as a potential novel target for therapeutics. Currently, faecal microbial transplantation, dietary interventions, use of probiotics, prebiotics and drugs are the major therapeutic tools utilized to impact dysbacteriosis and associated intestinal diseases. In this review, we systematically summarized the role of intestinal microbiome in the occurrence and development of intestinal diseases. The potential mechanism of the complex interplay between gut dysbacteriosis and intestinal diseases, and the treatment methods are also highlighted.

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A Potential Role of Salmonella Infection in the Onset of Inflammatory Bowel Diseases

Cited by 74 publications

References 137 publications

GiardiaInfection of the Small Intestine Induces Chronic Colitis in Genetically Susceptible Hosts

GiardiaInfection of the Small Intestine Induces Chronic Colitis in Genetically Susceptible Hosts

Gut microbiota in the pathogenesis of inflammatory bowel disease

Gut dysbacteriosis and intestinal disease: mechanism and treatment

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