Invasiveness of <i>Helicobacter pylori</i> into Human Gastric Mucosa

Ko, Gyung Hyuck; Kang, Seung Goo; Kim, You Kyung; Lee, Jeong-Hee; Park, Cheol Keun; Youn, Hee Shang; Baik, Seung‐Chul; Cho, Myung Je; Lee, Woo Kon; Rhee, Kwang Ho

doi:10.1046/j.1523-5378.1999.98690.x

Cited by 35 publications

(27 citation statements)

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“…While the majority of H. pylori remain in the intestinal lumen, H. pylori can also be found within gastric epithelial cells. Recently, H. pylori have also been described within metaplastic, dysplastic, and neoplastic gastric epithelial cells in vivo [15][16][17][18][19][20], and it has been suggested that the intracellular expression of H. pylori virulence genes might play a role in the development of H. pylori associated diseases [19].…”

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confidence: 99%

Adherence, Internalization, and Persistence of Helicobacter pylori in Hepatocytes

et al. 2008

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Although Helicobacter pylori have been identified in the liver, the role of Helicobacter sp. in human liver diseases remains unclear. This study explored whether H. pylori were internalized and could persist in hepatocytes. The majority of an inoculum of H. pylori (1 × 10 7 colony forming units) adhered to hepatocytes. Using the gentamicin invasion assay we found that approximately 2% were internalized and persisted following passage for more than 2 months. Electron microscopy confirmed the presence of intracellular Helicobacter. The number of adherent or internalized H. pylori was significantly greater with hepatocytes than with gastric epithelial cells (P <0.05) and was also dependent on cag pathogenicity island (PAI), VacA, OipA, or BabA status. Transmission electron microscopy was used to confirm adherence and invasion of H. pylori into hepatocytes. Internalization of H. pylori was inhibited by antibodies to β1-integrin receptors, genistein, and cytochalasin D (P < 0.05) consistent with β1-integrin acting as a surface receptor with additional requirements for tyrosine kinase phosphorylation and actin polymerization. In summary, H. pylori both adhered to and invaded into hepatocytes in vitro, depending on the virulent factors, and persisted within hepatocytes during subcultures. β1-integrin is likely a receptor involved in internalization of H. pylori into hepatocytes.

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confidence: 99%

Adherence, Internalization, and Persistence of Helicobacter pylori in Hepatocytes

et al. 2008

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“…18 The invasion of H. pylori into the lamina propria was confirmed by immunoelectron microscopy. 19,20 These observations that H. pylori invades the gastric mucosa have not been integrated into the pathogenesis of H. pylori-associated gastritis, however, even in recent reviews, 1,3,11 but the presence of H. pylori in the lamina propria may be an important factor in the induction and development of gastric inflammation. H. pylori invasion of the lamina propria stimulates the mucosal inflammatory cells more intensely than does the bacterium attached to the epithelial cells.…”

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

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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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“…H. pylori resides extracellularly within the gastric mucus layer of the human stomach, with only 1% of the organisms attached to host epithelial cells (11). The normal gastric mucosa of H. pylori-negative adults and children is populated by very few macrophages (12).…”

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Macrophages Are Mediators of Gastritis in Acute Helicobacter pylori Infection in C57BL/6 Mice

et al. 2008

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Helicobacter pylori is the etiological agent of human chronic gastritis, a condition seen as a precursor to the development of gastrointestinal ulcers or gastric cancer. This study utilized the murine model of chronic H. pylori infection to characterize the role of macrophages in the induction of specific immune responses and gastritis and in the control of the bacterial burden following H. pylori infection and vaccination. Drug-loaded liposomes were injected intravenously to deplete macrophages from C57BL/6 mice, and effective removal of CD11b ؉ cells from the spleens and stomachs of mice was confirmed by immunofluorescence microscopy. Transient elimination of macrophages from C57BL/6 mice during the early period of infection reduced the gastric pathology induced by H. pylori SS1 but did not affect the bacterial load in the stomach. These data suggest that macrophages are important to the severity of gastric inflammation during H. pylori infection.

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Invasiveness of Helicobacter pylori into Human Gastric Mucosa

Abstract: H. pylori rarely invade the lamina propria and gastric cells.

Cited by 35 publications

References 11 publications

Adherence, Internalization, and Persistence of Helicobacter pylori in Hepatocytes

Adherence, Internalization, and Persistence of Helicobacter pylori in Hepatocytes

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

Macrophages Are Mediators of Gastritis in Acute Helicobacter pylori Infection in C57BL/6 Mice

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