Hepatic inflammation in rats with experimental small intestinal bacterial overgrowth

Lichtman, Steven N.; Sartor, R. Balfour; Keku, J; Schwab, John H.

doi:10.1016/0016-5085(90)90833-m

Cited by 203 publications

(96 citation statements)

References 32 publications

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“…For e�a��le, animal studies demonstrate a correlation between bacteri� al overgrowth and bacterial translocation. Experimentally induced bacterial overgrowth results in bacterial translo� cation, liver injury, and inflammation [50] . In addition, as we have discussed above, selective intestinal deconta�ina� tion i��roves e��eri�ental alcoholic steatohe�atitis.…”

Section: Microfloramentioning

confidence: 99%

Bacterial translocation and changes in the intestinal microbiome associated with alcoholic liver disease

Yan¹

2012

WJH

101

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Alcoholic liver disease progresses through several stages of tissue damage, from simple steatosis to alcoholic hepatitis, fibrosis, or cirrhosis. Alcohol also affects the intestine, increases intestinal permeability and changes the bacterial microflora. Liver disease severity correlates with levels of systemic bacterial products in patients, and experimental alcoholic liver disease is dependent on gut derived bacterial products in mice. Supporting evidence for the importance of bacterial translocation comes from animal studies demonstrating that intestinal decontamination is associated with decreased liver fibrogenesis. In addition, mice with a gene mutation or deletion encoding receptors for either bacterial products or signaling molecules downstream from these receptors, are resistant to alcohol-induced liver disease. Despite this strong association, the exact molecular mechanism of bacterial translocation and of how changes in the intestinal microbiome contribute to liver disease progression remains largely unknown. In this review we will summarize evidence for bacterial translocation and enteric microbial changes in response to alcoholic liver injury and chronic alcoholic liver disease. We will further describe consequences of intestinal dysbiosis on host biology. We finally discuss how therapeutic interventions may modify the gastrointestinal microflora and prevent or reduce alcoholic liver disease progression

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Section: Microfloramentioning

confidence: 99%

Bacterial translocation and changes in the intestinal microbiome associated with alcoholic liver disease

Yan¹

2012

WJH

101

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“…In addition, overgrowth of predominantly anaerobic bacteria in bypassed small intestinal segments can lead to systemic inflammation. A jejunal self-filling blind loop induces hepatobiliary inflammation resembling sclerosing cholangitis and reactivates quiescent arthritis in genetically susceptible Lewis or Wistar rats (24,25), and some patients undergoing surgical treatment for morbid obesity with creation of bypassed jejunoileal segments develop arthritis and hepatic and skin inflammation (8). In both examples, metronidazole or broad-spectrum antibiotics with anaerobic specificities can reverse these systemic manifestations (15,23,25).…”

mentioning

confidence: 99%

Different Subsets of Enteric Bacteria Induce and Perpetuate Experimental Colitis in Rats and Mice

Rath

Schultz

Freitag³

et al. 2001

Infect Immun

310

220

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Resident bacteria are incriminated in the pathogenesis of experimental colitis and inflammatory bowel diseases. We investigated the relative roles of various enteric bacteria populations in the induction and perpetuation of experimental colitis. HLA-B27 transgenic rats received antibiotics (ciprofloxacin, metronidazole, or vancomycin-imipenem) in drinking water or water alone in either prevention or treatment protocols. Mice were treated similarly with metronidazole or vancomycin-imipenem before or after receiving 5% dextran sodium sulfate (DSS). Germfree transgenic rats were colonized with specific-pathogen-free enteric bacteria grown overnight either in anaerobic or aerobic atmospheres. Nontransgenic rats colonized with anaerobic bacteria served as negative controls. Although preventive metronidazole significantly attenuated colitis in transgenic rats and DSS-treated mice, it had no therapeutic benefit once colitis was established. Ciprofloxacin also partially prevented but did not treat colitis in B27 transgenic rats. In both animal models vancomycinimipenem most effectively prevented and treated colitis. Germfree transgenic rats reconstituted with enteric bacteria grown under anaerobic conditions had more aggressive colitis than those associated with aerobic bacteria. These results suggest that a subset of resident luminal bacteria induces colitis, but that a complex interaction of commensal aerobic and anaerobic bacteria provides the constant antigenic drive for chronic immune-mediated colonic inflammation.Rapidly growing evidence supports the influence of normal enteric bacteria on the pathogenic process of intestinal inflammation and extraintestinal manifestations in experimental colitis and human inflammatory bowel diseases (IBD) (40-43). Both spontaneous and induced inflammation in multiple widely diverse rodent models have been associated with commensal luminal bacteria (1, 11-13, 16, 22, 31, 44, 45, 52, 54). The influence of resident bacteria on the induction and perpetuation of spontaneous colitis and gastritis has been thoroughly studied in HLA-B27/␤ 2 -microglobulin transgenic (B27 TG) rats. Colitis, gastritis, and joint inflammation fail to develop in B27 TG rats raised under germfree (sterile) conditions (36, 49). Moreover, when transferred into a specific-pathogenfree (SPF) environment, B27 TG rats universally develop immune-mediated colitis and gastritis within 1 month of bacterial colonization (36).However, not all luminal bacteria have equal abilities to cause inflammation. Antibiotics with narrow specificities, such as metronidazole, which is selectively active against anaerobic bacteria, are effective in Crohn's colitis and ileocolitis (47) and also attenuate chronic experimental intestinal inflammation induced by indomethacin or carageenan in rats and guinea pigs, respectively (32, 54). In addition, overgrowth of predominantly anaerobic bacteria in bypassed small intestinal segments can lead to systemic inflammation. A jejunal self-filling blind loop induces hepatobiliary inflammation rese...

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“…[6][7][8][9][10] In PSC, bacterial translocation from the gut to the liver is hypothesized to play a major role in disease development, and from animal studies it is known that bacterial translocation in rats induces PSC-like changes. 11 Multi-tagged pyrosequencing analyses of stool samples from patients with liver cirrhosis showed progressive changes in the gut microbiome characterized by a significant increase in Clostridiales XIV (Ruminococcaceae and Lachnospiraceae) and a decrease in Enterococcaeae, Staphylococcaceae, and Enterobacteriaceae compared with controls. 12 To date, there are no data available on the intestinal microbiota in cholestatic liver diseases, apart from cirrhotic liver disease.…”

Section: Introductionmentioning

confidence: 99%

The Mucosa-associated Microbiota of PSC Patients is Characterized by Low Diversity and Low Abundance of Uncultured Clostridiales II

Rossen

Fuentes

Boonstra

et al. 2014

Journal of Crohn's and Colitis

112

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Background: Primary sclerosing cholangitis (PSC) is a cholestatic liver disease that is strongly associated with a particular phenotype of inflammatory bowel disease (IBD) with right-sided colonic involvement. In IBD, several studies demonstrated significant aberrancies in the intestinal microbiota in comparison with healthy controls. We aimed to explore the link between IBD and PSC by studying the intestinal mucosa-adherent microbiota in PSC and ulcerative colitis (UC) patients and noninflammatory controls. Methods: We included 12 PSC patients, 11 UC patients, and nine noninflammatory controls. The microbiota composition was determined in ileocecal biopsies from each patient by 16S rRNAbased analyses using the human intestinal tract chip. Results: Profiling of the mucosa-adherent microbiota of PSC patients, UC patients, and noninflammatory controls revealed that these groups did not cluster separately based on microbiota composition. At the genus-like level, the relative abundance of uncultured Clostridiales II was significantly lower (almost 2-fold) in PSC (0.26 ± 0.10%) compared with UC (0.41 ± 0.29%) and controls (0.49 ± 0.25%) (p = 0.02). Diversity and richness in the microbiota composition differed across the groups and were significantly lower in PSC patients compared with noninflammatory controls (p = 0.04 and p = 0.02, respectively). No significant differences were found in evenness. Conclusions: Reduced amounts of uncultured Clostridiales II in PSC biopsies in comparison with UC and healthy controls can be considered a signature of a compromised gut, as we have recently observed that this group of as yet uncultured Firmicutes correlates significantly with health.

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Hepatic inflammation in rats with experimental small intestinal bacterial overgrowth

Cited by 203 publications

References 32 publications

Bacterial translocation and changes in the intestinal microbiome associated with alcoholic liver disease

Bacterial translocation and changes in the intestinal microbiome associated with alcoholic liver disease

Different Subsets of Enteric Bacteria Induce and Perpetuate Experimental Colitis in Rats and Mice

The Mucosa-associated Microbiota of PSC Patients is Characterized by Low Diversity and Low Abundance of Uncultured Clostridiales II

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