Duodenal bacterial load as determined by quantitative polymerase chain reaction in asymptomatic controls, functional gastrointestinal disorders and inflammatory bowel disease

2020 ◽  
Vol 52 (1) ◽  
pp. 155-167
Author(s):  
Ayesha Shah ◽  
Nicholas J. Talley ◽  
Natasha Koloski ◽  
Graeme A. Macdonald ◽  
Bradley J. Kendall ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Polymerase Chain Reaction ◽  
Bowel Disease ◽  
Quantitative Polymerase Chain Reaction ◽  
Bacterial Load ◽  
Functional Gastrointestinal Disorders ◽  
Gastrointestinal Disorders ◽  
Chain Reaction ◽  
Inflammatory Bowel ◽  
Polymerase Chain

Diagnosing cytomegalovirus in patients with inflammatory bowel disease—by immunohistochemistry or polymerase chain reaction?

2015 ◽  
Vol 466 (5) ◽  
pp. 533-539 ◽  
Author(s):  
Nina Zidar ◽  
Ivan Ferkolj ◽  
Katja Tepeš ◽  
Borut Štabuc ◽  
Nika Kojc ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Polymerase Chain Reaction ◽  
Bowel Disease ◽  
Chain Reaction ◽  
Inflammatory Bowel ◽  
Polymerase Chain

Periodontitis Salivary Microbiota Worsens Colitis

2021 ◽  
pp. 002203452110497
Author(s):  
J. Qian ◽  
J. Lu ◽  
Y. Huang ◽  
M. Wang ◽  
B. Chen ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Polymerase Chain Reaction ◽  
Real Time ◽  
Bowel Disease ◽  
Chain Reaction ◽  
Salivary Microbiota ◽  
Inflammatory Bowel ◽  
Polymerase Chain

Evidence suggests that periodontitis contributes to the pathogenesis of inflammatory bowel disease, including Crohn’s disease and ulcerative colitis. However, few studies have examined the role of swallowing and saliva in the pathogenesis of gastrointestinal diseases. Saliva contains an enormous number of oral bacteria and is swallowed directly into the intestine. Here, we explored the influence of periodontitis salivary microbiota on colonic inflammation and possible mechanisms in dextran sulfate sodium (DSS)–induced colitis. The salivary microbiota was collected from healthy individuals and those with periodontitis and gavaged to C57BL/6 mice. Periodontitis colitis was induced by DSS for 5 d and ligature for 1 wk. The degree of colon inflammation was evaluated through hematoxylin and eosin staining, ELISA, and quantitative real-time polymerase chain reaction. Immune parameters were measured with quantitative real-time polymerase chain reaction, flow cytometry, and immunofluorescence. The gut microbiota and metabolome analyses were performed via 16S rRNA gene sequencing and liquid chromatography–mass spectrometry. Although no significant colitis-associated phenotypic changes were found under physiologic conditions, periodontitis salivary microbiota exacerbated colitis in a periodontitis colitis model after DSS induction. The immune response more closely resembled the pathology of ulcerative colitis, including aggravated macrophage M2 polarization and Th2 cell induction (T helper 2). Inflammatory bowel disease–associated microbiota, such as Blautia, Helicobacter, and Ruminococcus, were changed in DSS-induced colitis after periodontitis salivary microbiota gavage. Periodontitis salivary microbiota decreased unsaturated fatty acid levels and increased arachidonic acid metabolism in DSS-induced colitis, which was positively correlated with Aerococcus and Ruminococcus, suggesting the key role of these metabolic events and microbes in the exacerbating effect of periodontitis salivary microbiota on experimental colitis. Our study demonstrated that periodontitis contributes to the pathogenesis of colitis through the swallowing of salivary microbiota, confirming the role of periodontitis in systemic disease and providing new insights into the etiology of gastrointestinal inflammatory diseases.

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