Proposed Mechanisms for the Translocation of Intestinal Bacteria

Wells, Carol L.; Maddaus, Michael A.; Simmons, Richard L.

doi:10.1093/clinids/10.5.958

Cited by 382 publications

(180 citation statements)

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“…25 Some believe that bacterial translocation may be a normal event, rather than a disease process, that is necessary to allow the gutassociated lymphoid tissue to generate immunocompetent cells. 26 In patients with gastric cancer, the normal mucosal barrier of the stomach may be disrupted by malignant tissue, but in the present study, positive culture was not correlated with the clinicopathologic data, including ulceration of the tumor and lymph node metastasis (data not shown). Because the H. pylori effector molecule VacA causes massive vacuolar degeneration of the epithelial cells, thus disrupting the gastric epithelial barrier, it is likely that translocation occurs in H. pylori-infected persons even without gastric cancer.…”

Section: Intestinal Metaplasiacontrasting

confidence: 70%

Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes

Ito

Kobayashi

Uchida

et al. 2008

Laboratory Investigation

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Helicobacter pylori has been considered to be non-invasive and to rarely infiltrate the gastric mucosa, even though there is an active Th1 immune response in the lamina propria of the H. pylori-infected stomach. To elucidate whether H. pylori invades the lamina propria and translocates to the gastric lymph nodes, we examined H. pylori in formalin-fixed and paraffin-embedded tissue sections of stomach and gastric lymph nodes obtained from 51 cancer patients using real-time PCR and immunohistochemistry (IHC) with a novel anti-H. pylori monoclonal antibody that recognizes lipopolysaccharides. Fresh gastric lymph nodes were used to culture for H. pylori. In 46 patients with H. pylori in the stomach, the bacterium was found in the lymph nodes from 21 patients by culture, 37 patients by PCR, and 29 patients by IHC. H. pylori captured by macrophages was found in the lamina propria of 39 patients. In the lymph nodes, the bacterium was found in many macrophages and a few interdigitating dendritic cells at the paracortical areas. H. pylori was also found in the intracellular canaliculi of parietal cells in 21 patients, but intracytoplasmic invasion into gastric epithelial cells was not identified. When compared to the commercially available anti-H. pylori antibodies, the novel antibody showed the highest sensitivity to detect H. pylori-positive macrophages, whereas no difference was found for H. pylori in the mucous layer. The H. pylori-positive macrophages in the lamina propria correlated with chronic gastritis as well as translocation of such cells to the lymph nodes. These results suggest that H. pylori-induced gastric epithelial damage allows the bacteria to invade the lamina propria and translocate to the gastric lymph nodes, which may chronically stimulate the immune system. The bacteria captured by macrophages, whether remaining alive or not, may contribute to the induction and development of H. pylori-induced chronic gastritis.

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Section: Intestinal Metaplasiacontrasting

confidence: 70%

Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes

Ito

Kobayashi

Uchida

et al. 2008

Laboratory Investigation

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“…In addition to transmission to the blood by the previously described routes, E. coli are known to translocate easily (7). Translocation is defined by Berg and Garlington (8) as the passage of viable bacteria from the gastrointestinal tract to the mesenteric lymph nodes and possibly other organs.…”

Section: Discussionmentioning

confidence: 99%

Sepsis Caused by Food-borne Infection with Escherichia coli

et al. 2005

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We report a case of sepsis caused by Escherichia coli (E. coli) of serotype O-143. A 78-year-old man developed symptoms of gastroenteritis after ingesting raw meat on noodles. He rapidly developed respiratory failure. Blood culture grew E. coli. The sepsis seemed to have directly spread from a food-borne infection. The development of primary sepsis after ingesting E. coli is very rare. We suspect that bacterial translocation played a major role. Serotype O-143 is recognized in enteroinvasive E. coli (EIEC) as well as in Shigella dysenteriae. The pathogen in the present case is suspected of being EIEC although the isolated E. coli strain was negative for the inv and ipa genes.

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“…Each inoculum was prepared as described above and the total number of viable bacteria suspended in 0.25 ml sterile saline was (1)(2)(3)(4)(5)x lo8. In each of two replicate experiments, four mice from each group were killed 15 min and 1,4,24 and 48 h after bacterial injection.…”

Section: In-uivo Clearance Of Bacteria By the Kidneys Spleen And Lioermentioning

confidence: 99%

Interactions of Escherichia coli and Proteus mirabilis with mouse mononuclear phagocytes

Wells

Jechorek

Nelson

1990

Journal of Medical Microbiology

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Summary. Five strains of enterobacteria (three of Escherichia coli and two of Proteus mirabilis) were studied to assess and compare their phagocytic uptake and intracellular killing by mouse macrophages. Each strain was injected intraperitoneally into separate groups of mice and peritoneal exudate cells were harvested after 3 min for phagocytosis to occur in vivo. Acridine orange staining showed that there were approximately 1 0-fold fewer intracellular P. mirabilis than E. coli cells. The average numbers of viable intracellular bacteria per leucocyte were 0.03 and 0.02 for P. mirabilis strains M 13 and H 1, respectively, and 0.48, 0.45, and 0.28 for E. coli strains M 14, A-D M5 and H40. Thus, both P. mirabilis strains were ingested less readily than any of the three E. coli strains (p

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Proposed Mechanisms for the Translocation of Intestinal Bacteria

Cited by 382 publications

References 0 publications

Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes

Helicobacter pylori invades the gastric mucosa and translocates to the gastric lymph nodes

Sepsis Caused by Food-borne Infection with Escherichia coli

Interactions of Escherichia coli and Proteus mirabilis with mouse mononuclear phagocytes

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