Use of the mouse for the isolation and investigation of stomach-associated, spiral-helical shaped bacteria from man and other animals

Dick, Elizabeth; Lee, A.; Watson, George F.; Jani, O'Rourke

doi:10.1099/00222615-29-1-55

Cited by 63 publications

(23 citation statements)

References 4 publications

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“…Recently Dick et aZ. 25 used mouse inoculation as a means of maintaining non-cultivable gastric spiral bacteria. Employing this method in another series of pigs, we detected "G. suis" in some animals that were negative for this micro-organism by the urease test and carbol fuchsin staining (unpublished results).…”

Section: Discussionmentioning

confidence: 99%

Histopathological study of porcine gastric mucosa with and without a spiral bacterium ("Gastrospirillum suis")

Mendes¹,

Queiroz²,

Rocha³

et al. 1991

Journal of Medical Microbiology

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Summary. Tightly spiralled bacteria ("Gastrospirillum suis") were seen in the pyloric mucosa of the stomach of 13 (104%) of 120 pigs that appeared clinically healthy at slaughter and in the fundic mucosa of three (5.0%) out of 60 pigs. The spiral organism could not be cultured from any pig. Chronic gastritis was observed in the pyloric mucosa of 53 (44.2%) of 120 pigs and in the fundic mucosa of 7 (1 1.7%) of 60 pigs. The 13 pigs with spiral bacteria in the pyloric region comprised one animal (7.7%) with normal pyloric mucosa, two (15.4%) with "borderline gastritis", and 10 (76.9%) with chronic gastritis-in one instance accompanied by signs of activity (numerous polymorphonuclear cells). The three pigs with spiral bacteria in the fundic mucosa comprised two animals with a normal fundic region and one with "borderline gastritis". The presence of the spiral bacterium was significantly associated with pyloric gastritis (p = 0.01 3) and with numbers of lymphoid follicles (p = 0.014).

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Section: Discussionmentioning

confidence: 99%

Histopathological study of porcine gastric mucosa with and without a spiral bacterium ("Gastrospirillum suis")

Mendes¹,

Queiroz²,

Rocha³

et al. 1991

Journal of Medical Microbiology

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“…In the second experiment done in Sydney a larger cage was used and 20 adult H. felis infected UNSW-SPF mice were mixed with 20 uninfected mice for 8 weeks. Results are shown in Table 1 Infection was carried out as described previously [14]. The contents were removed 104 A. LEE AND OTHERS from the glandular region of three stomachs of infected mice.…”

Section: Transmission Between H Felis Infected and Uninfected Adult mentioning

confidence: 99%

“…In two separate experiments CD 1 mice were infected with the gastric homogenates of Australian mice containing 'Gastrospirillum hominis' and the natural murine yeast Torulopsis pintolopesii. This yeast, which is easily visible on the glandular gastric mucosa is the normal flora of the conventional mice which were used to first isolate 'Gastrospirillum hominis' [14]. The CD1-SPF mice did not have this yeast as part of their normal flora; thus whenever CD1 mice were colonized with the 'Gastrospirillum' via stomach homogenate the yeast transferred as well.…”

Section: Transmission Between H Felis Infected and Uninfected Adult mentioning

confidence: 99%

“…Since that time human infection with this agent has been reported from many parts of the world. Although this bacterium cannot be cultured in vivo we have managed to maintain it invivo by feeding human gastric biopsy specimens to mice [14]. Heavy 5 ,ag/ml (Sigma), polymyxin B 3 ,ug/ml (Sigma) and amphotericin [2][3][4][5] ,ug/ml lot (Fungizone; Squibb) for 48 h at 370 under microaerophilic conditions as previously described [10].…”

Section: Introductionmentioning

confidence: 99%

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Transmission ofHelicobacterspp. A challenge to the dogma of faecal-oral spread

et al. 1991

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SUMMARYFaecal oral spread is claimed by many to be the mode of transmission of the gastric pathogenHelicobacter pylori. This idea is based not on experimental data but because the epidemiology ofH. pyloriinfection resembles that of other pathogens known to be spread by the faecal-oral route. This is in spite of the observation that no-one has been successful in culturingH. pylorifrom human stool. In this study, a series of transmission experiments are reported on animals infected with the gastric spirilla,Helicobacter felisand ‘Gastrospirillum hominis’. Germfree mice and rats infected withH. felisdid not transmit their infection to uninoculated mice despite prolonged contact in the same cage nor could the bacterium be isolated from their intestinal contents. This was confirmed in specific pathogen free mice where infected dams did not pass the helicobacter to their progeny. Similarly, mice infected with a human isolate of ‘Gastrospirillum hominis’ did not transmit the infection while in close contact with uninoculated mice. In contrast, in a limited series of experiments, bothH. pyloriandH. feliswere transmitted from infected gnotobiotic Beagle puppies to uninfected animals in the same enclosure. In addition, the gastric mucus from a cat with indigenous ‘Gastrospirillum’-like organisms was infectious for mice, whereas faecal content from the same animal was not. It is suggested that the difference between the murine and canine experiments is that the dogs are more likely to have oral-oral contact than rodents. Unlike dogs, mice and rats do not vomit and are coprophagous. It is concluded that the case for faecal-oral spread ofHelicobacterspecies is ‘not proven’ and that the inter-oral route is more likely.

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“…H. felis is a gastric Helicobacter that colonizes the stomachs of laboratory mice, dogs, and cats and can induce active chronic gastritis that mimics the pathological features observed in H. pyroli-induced gastritis in humans (4,9,19,20,29). Next, we examined whether H. felis colonization can induce expression of TSLP in gastric epithelial cells.…”

Section: H Pylori Colonization Induces Tslp Expression In Human Gastmentioning

confidence: 99%

Helicobacter pylori Promotes the Production of Thymic Stromal Lymphopoietin by Gastric Epithelial Cells and Induces Dendritic Cell-Mediated Inflammatory Th2 Responses

et al. 2010

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Helicobacter pylori colonizes the stomach and induces strong, specific local and systemic humoral and cell-mediated immunity, resulting in the development of chronic gastritis in humans. Although H. pyloriinduced chronic atrophic gastritis is characterized by marked infiltration of T helper type 1 (Th1) cytokineproducing CD4؉ T cells, almost all of the inflamed gastric mucosae also contain focal lymphoid aggregates with germinal centers. In addition, typical H. pylori-induced chronic gastritis in children, called follicular gastritis, is characterized by B-cell follicle formation in the gastric mucosa. The aim of this study was to examine whether thymic stromal lymphopoietin (TSLP), an epithelial-cell-derived cytokine inducing a dendritic cell (DC)-mediated inflammatory Th2 response, is involved in Th2 responses triggering B-cell activation in H. pylori-induced gastritis. Here, we show that H. pylori triggered human gastric epithelial cells to produce TSLP, together with the DC-attracting chemokine MIP-3␣ and the B-cell-activating factor BAFF. After DCs were incubated with supernatants from H. pylori-infected epithelial cells, the conditioned cells expressed high levels of costimulatory molecules, such as CD80, and triggered naïve CD4؉ T cells to produce high levels of the Th2 cytokines interleukin-4 and interleukin-13 and of the inflammatory cytokines tumor necrosis factor alpha and gamma interferon. In contrast, after incubation of the supernatants with the neutralizing antibodies to TSLP, the conditioned DCs did not prime T cells to produce high levels of Th2 cytokines. These results, together with the finding that TSLP was expressed by the epithelial cells of human follicular gastritis, suggest that H. pylori can directly trigger epithelial cells to produce TSLP. It also suggests that TSLP-mediated DC activation may be involved in Th2 responses triggering B-cell activation in H. pylori-induced gastritis.Helicobacter pylori (H. pylori) infection in the stomach induces chronic gastritis associated with the development of peptic ulcer diseases, gastric adenocarcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma in humans (3,8,35). Although H. pylori-induced chronic atrophic gastritis is characterized by marked infiltration of T helper type 1 (Th1) cytokine-producing CD4 ϩ T cells (3,8,35), almost all of the inflamed gastric mucosae also contain focal lymphoid aggregates with germinal centers (5, 11). In addition, typical H. pylori-induced chronic gastritis in children, called follicular gastritis, is characterized by B-cell follicle formation in the gastric mucosa (10,11,34). Th2 responses triggering B-cell activation appear to be involved in the development of lymphoid aggregates with germinal centers. However, molecular mechanisms to induce Th2 responses triggering B-cell activation are not clear.In humans, an epithelial-cell-derived cytokine, thymic stromal lymphopoietin (TSLP), activates CD11c ϩ myeloid dendritic cells (DCs), and activated DCs strongly upregulate the expression of costimulatory mo...

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Use of the mouse for the isolation and investigation of stomach-associated, spiral-helical shaped bacteria from man and other animals

Cited by 63 publications

References 4 publications

Histopathological study of porcine gastric mucosa with and without a spiral bacterium ("Gastrospirillum suis")

Histopathological study of porcine gastric mucosa with and without a spiral bacterium ("Gastrospirillum suis")

Transmission ofHelicobacterspp. A challenge to the dogma of faecal-oral spread

Helicobacter pylori Promotes the Production of Thymic Stromal Lymphopoietin by Gastric Epithelial Cells and Induces Dendritic Cell-Mediated Inflammatory Th2 Responses

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