Helicobacter Heilmannii Infection Research Articles

The Relationship of a Helicobacter heilmannii Infection to the Mucosal Changes in Abattoir and Laboratory Pig Stomach

A pig ulcer model in which ulceration is reproducibly induced in the pars oesophagea (a tongue of the oesophageal squamous epithelium that extends into the pig stomach) by bile duct ligation (BDL) was used in this study to determine whether Helicobacter heilmannii (Hh) is a predisposing factor in the ulceration of this region. The infection with Hh and its relationship to ulceration and mucus integrity was examined. We microscopically investigated the occurrence of spontaneous pars oesophageal ulceration in 33 pigs from a local abattoir and 5 pigs nurtured in pens in our surgical laboratory (JSM). Further groups of 5 and 6 JSM pigs underwent a sham operation and a BDL, respectively. Giemsa staining was used to detect Hh and purified mucin was characterized by gel filtration. Ten of 33 and 2 of 5 of the stomachs of abattoir and JSM pigs, respectively, were positive for Hh by Giemsa stain. Three of the 33 abattoir pigs showed ulceration in the pars oesophagea and none of these was Hh-positive. All six of the bile duct-ligated pigs showed ulceration in the pars but only 2 of these were Giemsa-positive. Only 8 of 33 of the abattoir pigs had > or =50% large polymeric mucin that was eluted in the void/excluded volume of a Sepharose 2B column. There was no consistent correlation between an infection of the pig stomachs by Hh, an ulceration of the pars oesophagea, and mucin degradation. There was a significant difference between the percentage of polymeric mucin from the abattoir pigs and that of the JSM group (P < 0.003), the JSM group vs sham-operated pigs (P < 0.011), and JSM vs BDL pigs (P < 0.0005), but there appeared to be no association between the infectivity with Hh and mucin degradation.

Helicobacter heilmannii gastroduodenal disease and clinical aspects in children with dyspeptic symptoms

To evaluate the occurrence and clinical characteristics of Helicobacter heilmannii infection among children presenting with dyspeptic symptoms. Prospective cohort study of 580 patients. Of all examined dyspeptic children, 26.4% were infected with spiral-shaped organisms, and 0.9% of patients were found to be infected with spiral H. heilmannii-like organisms. In children with dyspeptic symptoms, the possible presence of gastroduodenal disease due to H. heilmannii should be considered. Further studies are needed to clarify H. heilmannii-related gastroduodenal pathology in the paediatric population.

Persistent increase in myofibroblasts in Helicobacter heilmannii-infected mice but not in Helicobacter pylori-infected Mongolian gerbils: colocalization of COX-2 and bFGF immunoreactivity.

The clinical significance of Helicobacter heilmannii infection remains uncertain, owing to the lack of a specific detection method. Recently, we reported a marked increase in myofibroblasts in the early stage of Helicobacter pylori infection in Monglian gerbils. The present study was designed to clarify changes in myofibroblasts, and in the immunoeactivities of basic fibroblast growth factor, cyclooxygenase-2 and inducible nitric oxide synthase after H. pylori infection in Monglian gerbils and H. heilmannii infection in mice. After oral inoculation, changes in the location of bacteria and the immunoreactivity of myofibroblasts, basic fibroblast growth factor, cyclooxygenase-2 and inducible nitric oxide synthase were stained with the indirect immunofluorescent method and observed by confocal laser microscopy. In H. heilmannii-infected mice, the increases in myofibroblasts and in immunoreactivities of these three markers were sustained 12 months after infection. In H. pylori-infected Monglian gerbils, however, these increases were significant at 3 months but had returned to control levels at 12 months. Two types of Helicobacter infection showed different patterns of myofibroblast proliferation, coinciding with the extent of inflammation. These findings suggest that this difference may be related to the consequences of the infection.

Cellular immune responses in Helicobacter heilmannii infection: evaluation of the role of the host and the bacterium.

We evaluated some aspects of the immune response to Helicobacter heilmannii in two mouse strains. Gastritis that was more severe in infected C57BL/6 mice. A proliferative response to H. pylori antigens was observed in splenocytes from H. heilmannii-positive and -negative mice, similar in the positive- and negative-BALB/c mice, but lower in the positive- than in the negative-C57BL/6 animals. A decrease in B cells and an increase in CD4+ cells after stimulation with type I H. pylori antigen and an increase in CD8+ cells after stimulation with type I and II antigens was observed in infected C57BL/6 mice. Conversely, the percentage of CD4+, CD8+, and B cells was similar in positive- and negative-BALB/c mice. These results demonstrated that the immune response is similar in H. heilmannii and H. pylori infection and strengthened the importance of host and bacterial virulence markers in the immune response to gastric Helicobacter infections.

The role of Th1 and Th2 immune response in Helicobacter heilmannii infection

The role of Th1 and Th2 immune response in Helicobacter heilmannii infection

The role of Th1 and Th2 immune response in Helicobacter heilmannii infection

The role of Th1 and Th2 immune response in Helicobacter heilmannii infection

Helicobacter heilmannii–associated primary gastric low-grade MALT lymphoma: Complete remission after curing the infection

Background & Aims: Cure of Helicobacter pylori infection may lead to complete remission of associated low-grade mucosa-associated lymphoid tissue (MALT) lymphoma in stage EI. This study investigated whether Helicobacter heilmannii infection–associated primary gastric MALT lymphoma will regress after cure of the infection. Methods: H. heilmannii–induced gastritis was diagnosed histologically, by a new specific immunoglobulin G enzyme-linked immunosorbent assay, and with 16S ribosomal RNA amplification and sequencing in 5 consecutive patients with primary gastric MALT lymphoma clinical stage EI. Patients received 40 mg omeprazole and 750 mg amoxicillin 3 times per day for 14 days. Polymerase chain reaction (PCR) was used to detect rearrangement of immunoglobulin heavy-chain genes before treatment and during follow-up. Results: Five patients (3 men, 2 women; mean age, 65 years; range, 42–79 years) were studied. H. pylori was not detected by culture, histology, serology, or PCR. Treatment resulted in the cure of H. heilmannii infection in each case and complete histological and endoscopic remission of the tumors. Three of 5 patients showed monoclonal B cells before treatment, 2 of whom remained PCR positive. Within a median follow-up period of 24 months, no relapse of the lymphoma or reinfection with H. heilmannii occurred. Conclusions: These data suggest that gastric MALT lymphoma may arise in patients with H. heilmannii infection. Cure of this infection may lead to complete remission of the MALT lymphoma. GASTROENTEROLOGY 2000;118:821-828

The relationships between chronic gastritis and gastric acid secretion.

Helicobacter pylori is the main cause of chronic gastritis in humans. Autoimmune mechanisms and Helicobacter heilmannii infection are other causes, both of which are of minor significance in a worldwide perspective. Atrophic gastritis is a quite common late consequence of H. pylori gastritis and will develop on a multifactorial basis, but not in all infected persons. The evolution of atrophic gastritis is a slow and gradually worsening process leading to subtypes, in which the antrum and corpus are affected to dissimilar extent and degree. The distal part of the stomach is the site where the atrophic sequelae (atrophic gastritis and intestinal metaplasia) of H. pylori infection occur most often. A minority of cases develop corpus-limited, or corpus-predominant atrophic gastritis. Along with the worsening of atrophic gastritis, inflammation and density of colonization of the mucosa by H. pylori tend to decrease in grade. In general, the degree of gastric mucosal inflammation, acute and chronic, is positively related to the degree of colonization of the mucosa by H. pylori. Acid secretion and local acidity are factors which modulate the ecology and density of colonization of H. pylori in the stomach, and may thus also modulate the evolution of chronic gastritis into topographically dissimilar subtypes. Acid secretion varies among individuals, this variation being perhaps caused by hereditary differences in parietal cell mass, or by differences in the sensitivity of parietal cells to hormonal or neural stimuli. It is hypothesized that in genuine hypersecretors, H. pylori colonization and subsequent gastritis with atrophic and metaplastic sequelae may be limited to the antrum, while in hyposecretors gastritis predominates in the corpus. In the latter, atrophic gastritis in the corpus then leads to further impairment of acid output. In these cases, H. pylori infection and gastritis may, finally, heal in the antrum, resulting in hypochlorhydria and atrophic gastritis that is limited to, or predominant in the corpus.