Helicobacter Heilmannii Infection Research Articles

Clinical aspects of Helicobacter heilmannii-associated gastritis in patients with dyspepsia: A systematic review and meta-analysis

BackgroundThe clinical relevance of Helicobacter heilmannii (H. heilmannii) infection in patients with upper gastrointestinal diseases is not yet fully understood. The main purpose of this study was to evaluate the clinical, endoscopic, histopathological, and therapeutic features of H. heilmannii. MethodsTo retrieve the relevant studies, we conducted a comprehensive systematic search of global databases such as the ISI Web of Science, PubMed, Scopus, Embase, and Google Scholar. After confirming the studies based on the inclusion criteria statistical analysis was performed using Comprehensive Meta-Analysis software. ResultsIn our study, the prevalence of infection with H. heilmannii was measured at 1.9% (95% CI: 0.8–4.2). The prevalence of H. heilmannii in Asian population was higher than Western countries (3.1% vs. 1.2%, respectively). Interestingly, the frequency of coinfection with both H. pylori and H. heilmannii was 15.4% (95% CI: 5.2–37.6). The most common endoscopic findings were chronic gastritis, hyperplasia, and erosion. In addition, our results showed that in people infected with this bacterium, gastric inflammation is typically chronic, focal, and less active than Helicobacter pylori (H. pylori) gastritis. Conventional treatment of H. pylori can lead to the eradication of H. heilmannii. ConclusionIn general, H. heilmannii infection is significantly associated with mild chronic gastritis and can be treated with standard anti-H. pylori treatment.

Two Cases of Gastric Mucosa-Associated Lymphoid Tissue Lymphoma With Helicobacter heilmannii Infection

Helicobacter heilmannii (H. heilmannii)-associated gastric mucosa-associated lymphoid tissue (MALT) lymphoma have been reported, although rare. We describe here two cases of H. heilmannii-associated gastric MALT lymphoma. Case 1. A 50-year-old man presented with epigastralgia. Gastrointestinal endoscopy disclosed multiple gastric ulcerations in antrum. The endoscopic biopsy specimen suggested MALT lymphoma and bacteria were observed, which were larger and more tightly coiled than H. pylori. H. pylori was undetectable in histology and serum antibody test. He was treated with a 7-day course of triple therapy consisting of lansoprazole, amoxicillin, and clarithromycin. 2 months after eradication, CR was confirmed by endoscopic and histologic examinations. Four-years after eradication, there were no signs of MALT lymphoma recurrence on endoscopic finding and biopsy specimen. Case 2. A 43-year-old man visited our hospital for epigastralgia. Gastrointestinal endoscopy revealed multiple gastric ulcerations in the upper body and angle. The endoscopic biopsy specimen suggested MALT lymphoma. H. pylori was undetectable in a culture, urea breath test, H. pylori stool antigen test, and serum antibody test. H. heilmannii was positive by immunostaining and pseudo-positive by PCR. We performed eradication therapy with esomeprazole, amoxicillin, clarithromycin, and metronidazole for 7 days, and 2 months after the treatment, endoscopic gastrointestinal examination revealed that the multiple ulcer lesions had improved. Biopsy specimens demonstrated that the small lymphocytes had also decreased, but lymphoid nodules were present. Six months after eradication therapy, there were signs of MALT lymphoma recurrence on endoscopic finding and biopsy specimen. We performed radiation therapy, and CR was confirmed by endoscopic and histologic examinations. We presented two rare cases of H. heilmannii associated MALT lymphoma. Several reports described the effectiveness of eradication therapy for H. pylori-negative gastric MALT lymphoma. H. heilmannii infection may be closely associated with etiology of H. pylori-negative gastric MALT lymphoma.

Gastritis por Helicobacter heilmannii sensu lato: descripción de un caso y revisión de la literatura

Helicobacter heilmannii (H. heilmannii) infection is common in domestic animals but is rare in humans, in whom it can cause mild to moderate chronic gastritis. Its distinctive morphology allows a differential diagnosis with a Helicobacter pylori (H. pylori) infection. We present a case of chronic gastritis caused by H. heilmannii in a 17-year-old patient with symptoms of dyspepsia. Gastric antral biopsies showed moderate inflammatory infiltrate and long corkscrew-shaped spiral microorganisms, located in gastric pits as well as in the superficial mucus layer suggestive of H. heilmannii infection. These organisms were positive for anti-H. pylori antibody. The clinical and pathological features of H. heilmannii infection are discussed together with a review of the literature.

Alteration of angiogenesis in Helicobacter heilmannii‐induced mucosa‐associated lymphoid tissue lymphoma: Interaction with c‐Met and hepatocyte growth factor

The hepatocyte growth factor (HGF)/c-Met pathway has attracted attention in the formation of malignant tumors, as HGF secreted from the microcirculatory components as well as residing macrophages has been suggested to act on the c-Met receptors of cancer cells to decrease apoptosis and increase proliferation, invasion, and metastasis. The present study was undertaken to elucidate the interaction of the gastric, hepatic, and pulmonary mucosa-associated lymphoid tissue (MALT) lymphoma induced by Helicobacter heilmannii infection with c-Met and HGF. C57BL/6 female mice, infected with H. heilmannii for 3 months were used. The localization of the HGF, c-Met, and HGF activator immunoreactivities was observed by the indirect immunohistochemical methods. In addition, the effect of c-Met antibody and c-Met inhibitor, PHA-665752, was also investigated. c-Met immunoreactivity was found in the lymphocytes composing the MALT lymphoma, and HGF immunoreactivity was recognized mostly in the endothelial cells and macrophages in the MALT lymphoma. HGFA was localized on mesenchymal cells other than the lymphocytes. The administration of the antibody against c-Met or the c-Met inhibitor to the infected mice induced the significant suppression of hepatic and pulmonary MALT lymphoma, while the gastric MALT lymphoma showed only a tendency to decrease in size, while the active caspase 3 positive cells markedly decreased in the gastric, hepatic, and pulmonary MALT lymphoma after the treatment with the c-Met antibody or the c-Met antagonist. HGF and c-Met pathway were suggested to contribute to the lymphomagenesis in the MALT lymphoma after H. heilmannii infection.

Helicobacter heilmannii: A Rare Cause of Abdominal Pain

Introduction: A 44-year-old female was referred to gastroenterology clinic for abdominal pain for 6 months. The pain was aching in quality, 5/10 in intensity, and aggravated by oral intake. The pain was associated with belching. Past history included partial hysterectomy for enlarged uterus, a caesarean section and mitral regurgitation. Physical exam was unremarkable. Mild leukocytosis was seen on laboratory investigation. An upper endoscopy was performed, which revealed patchy erythema, friability, and granularity in the antrum (Figure 1-2). Histopathology confirmed chronic active gastritis, positive for Helicobacter organisms. H. Pylori immunostain highlighted numerous well-defined corkscrew organisms that were longer than typical H. pylori organisms, consistent with Helicobacter heilmannii. Helicobacter heilmannii (H. heilmannii) infection is a relatively rare causative agent of gastroduodenal diseease. However, H. heilmannii frequently colonizes gastric mucosa of animals, primarily cats and dogs, from where it can be transmitted to humans. Patients usually present with longstanding epigastric pain, nausea, vomiting, and heartburn. The patient was successfully treated with antibiotic therapy with resolution of symptoms.Figure 1Figure 2

Gastric de novo Muc13 expression and spasmolytic polypeptide-expressing metaplasia during Helicobacter heilmannii infection.

Helicobacter heilmannii is a zoonotic bacterium that has been associated with gastric disease in humans. In this study, the mRNA expression of mucins in the stomach of BALB/c mice was analyzed at several time points during a 1-year infection with this bacterium, during which gastric disease progressed in severity. Markers for acid production by parietal cells and mucous metaplasia were also examined. In the first 9 weeks postinfection, the mRNA expression of Muc6 was clearly upregulated in both the antrum and fundus of the stomach of H. heilmannii-infected mice. Interestingly, Muc13 was upregulated already at 1 day postinfection in the fundus of the stomach. Its expression level remained high in the stomach over the course of the infection. This mucin is, however, not expressed in a healthy stomach, and high expression of this mucin has so far only been described in gastric cancer. In the later stages of infection, mRNA expression of H(+)/K(+)-ATPase α/β and KCNQ1 decreased, whereas the expression of Muc4, Tff2, Dmbt1, and polymeric immunoglobulin receptor (pIgR) increased starting at 16 weeks postinfection onwards, suggesting the existence of spasmolytic polypeptide-expressing metaplasia in the fundus of the stomach. Mucous metaplasia present in the mucosa surrounding low-grade mucosa-associated lymphoid tissue (MALT) lymphoma-like lesions was also histologically confirmed. Our findings indicate that H. heilmannii infection causes severe gastric pathologies and alterations in the expression pattern of gastric mucins, such as Muc6 and Muc13, as well as disrupting gastric homeostasis by inducing the loss of parietal cells, resulting in the development of mucous metaplasia.

Helicobacter heilmannii Infection in a 43-Year-Old Female Effectively Treated with the Standard Triple Therapy

Helicobacter heilmannii Infection in a 43-Year-Old Female Effectively Treated with the Standard Triple Therapy

Su1665 Induced Expression of Cd86 in Gastric MALT Lymphoma by Helicobacter heilmannii Infection

as well as a reduced expression of CD80/CD86. Co-cultivation of allogenic T cells with H. pylori challenged MoDC results in an Interferon-γ secretion by T cells. However, the T cell response was modified when TLR-2 was neutralized. Conclusion: For the recognition of H. pylori by MoDC, TLR-2 plays an important role. When neutralized, MoDC induce stronger H. pylori specific T cell responses, although co-stimulatory activation markers on MoDC and secreted cytokines were reduced. The role of TLR subtypes therefore appears to have an important impact on regulation of T cell activation, andmechanisms are being investigated. Similar mechanism may account for other autoimmune diseases, which is of considerable clinical impact.

Su1674 Helicobacter heilmannii Infection: Clinical and Pathologic Characteristics of 160 Consecutive Cases Seen Over a 44-Month Period

Su1674 Helicobacter heilmannii Infection: Clinical and Pathologic Characteristics of 160 Consecutive Cases Seen Over a 44-Month Period

Molecular Mechanism of Gastric MALT Lymphoma Formation by Helicobacter heilmannii Infection

liver. Twelve and eighteen months after the infection, approximately 100% of infected mice had liver and pulmonary lesions. Some of the MALT lymphomas were defined as belonging to the high-grade group by the PCNA positivity. Eradication of the bacteria induced shrinkage of the tumor in the liver and the lung with apoptotic cells as well as in the stomach. Conclusion: Long-term infection with Helicobacter heilmannii in C57BL/6 mouse induced lowand high-grade hepatic and pulmonary MALT lymphoma as well as gastric lymphoma. Eradication of the bacteria brought about shrinkage of the hepatic and pulmonary lesions as well as gastric MALT lymphoma.

W1721 Helicobacter heilmannii Infection Induces Alteration of Stem Cell Environment as Well as Delayed Healing in Acetic Acid Ulcer

W1721 Helicobacter heilmannii Infection Induces Alteration of Stem Cell Environment as Well as Delayed Healing in Acetic Acid Ulcer

781 Effect of Celecoxib On the Suppression of Gastric Low-Grade MALT Lymphoma Induced By Helicobacter heilmannii Infection

781 Effect of Celecoxib On the Suppression of Gastric Low-Grade MALT Lymphoma Induced By Helicobacter heilmannii Infection

Microcirculatory alteration in low‐grade gastric mucosa‐associated lymphoma by Helicobacter heilmannii infection: Its relation to vascular endothelial growth factor and cyclooxygenase‐2

There are clinical reports that Helicobacter heilmannii, as well as Helicobacter pylori, has been clinically reported to cause gastric low-grade mucosa-associated lymphoid tissue-type (MALT) lymphoma, although its precise mechanism remains to be clarified. Thus, the present study was undertaken to elucidate the alteration of the microcirculatory structure and the relation to angiogenetic factors in mice infected with H. heilmannii for 3 and 6 months. Immunohistochemical studies have been performed by FITC-dextran intra-aortic infusion or CD31, vascular endothelial growth factor-A, cyclooxygenase 2 antibodies using our recently established model of gastric mucosa-associated lymphoid tissue-type gastric B-cell lymphoma in C57BL/6 mice. Increased microcirculatory network was recognized surrounding the MALT lymphoma tissues by both the FITC-dextran infusion method and CD31 immunoreactivity. Vascular endothelial growth factor-A immunoreactivity was recognized within the lymphoma tissues as well as in the marginal area, while cyclooxygenase-2 immunoreactivity was localized in the area surrounding the MALT lymphoma tissues. Increased microvascular network as well as enhanced VEGF-A immunoreactivity was shown to be related to expansion of the MALT lymphoma formed by Helicobacter heilmannii infection.

Gastric Helicobacter species as a cause of feline gastric lymphoma: A viable hypothesis

Gastric Helicobacter spp. are associated with chronic inflammation and neoplastic transformation in humans as well as domestic and laboratory species. The present study examined the association of Helicobacter heilmannii ( Hhe) infection in pet cats with feline gastric mucosa associated lymphoid tissue (MALT) lymphoma. Tissues were collected via gastric biopsy or at necropsy from 47 pet cats with clinical signs of gastrointestinal disease, including vomiting and inappetance, and classified as gastritis (14/47), lymphoma (31/37), or normal (2/47). Tissues positive for argyrophilic organisms with Warthin–Starry stain (29/47) were assessed by fluorescent in situ hybridization (FISH) for the presence of Hhe strains 1–4 as well as with a fifth probe that detected Helicobacter salomonis, Helicobacter bizzozeronii, or Helicobacter felis. A significant association of positive Warthin–Starry status with Hhe infection was found in cases of sick cats (22/29; p < 0.05 by Chi-square; χ 2 = 7.034). Interestingly, a significant association between Hhe status and a diagnosis of lymphoblastic or lymphocytic lymphoma was observed as well in a subset of 24 Warthin–Starry positive lymphoma cases: of lymphoblastic lymphoma cases, 13/17 were positive for Hhe ( p < 0.05; χ 2 = 4.854). Hhe strains 2 and 4 were most commonly found (18/29 and 17/29, respectively) among sick cats, although a higher than expected number of cats was also positive for Hhe1, which initial reports have described as rare in cats and common in humans. The association found between a positive Hhe status with the presence of feline gastric lymphoma, especially lymphoblastic lymphoma, argues for the need to conduct prospective studies to better identify the frequency and strain distribution of Hhe infection in both healthy and clinically ill cats, particularly those cats with gastric lymphoma.

A Report of Two Children withHelicobacter HeilmanniiGastritis and Review of the Literature

An 11-year-old boy with epigastric abdominal pain and a 2 year-old girl with failure to thrive underwent esophagogastroduodenoscopy. Endoscopic biopsies from the gastric antrum of both children revealed corkscrew-like spiral bacteria, consistent with the diagnosis of Helicobacter heilmannii infection. H. heilmannii is a rare finding in children and is thought to be present in approximately 0.3% of patients undergoing upper endoscopy. Clinical presentation, gross and histologic appearance, and treatment regimens are discussed. The clinical and histologic features of previously reported cases of H. heilmannii gastritis in children living in the United States are reviewed in table form.

Interaction of VEGF to gastric low grade MALT lymphoma by Helicobacter heilmannii infection in C57/BL/6 mice

Helicobacter heilmannii (Hh) has been clinically reported to have some relation to gastric low grade MALT lymphoma. Recently, we have formed the gastric MALT lymphoma in C57BL/6 mice. C57BL/6 mice infected with Hh from cynomolgus monkey for more than 6 months were used. The macroscopic, immunohistochemical and electron microscopic observation was performed MALT lymphoma was formed in almost 100% of the infected mice. Increased VEGF-A and Flt-3 immunoreactivity was recognized. Hh was shown to be related to the formation of MALT lymphoma and VEGF is suggested to play a role in this lymphoma.

Acute Phlegmonous Gastritis Associated with Helicobacter heilmannii Infection in a Child

Acute phlegmonous gastritis is a rare, rapidly progressive suppurative bacterial infection of the wall of the stomach. Two types are described, a diffuse type, in which the whole stomach is involved, and a localized type, in which a part of the stomach, usually the antrum, is affected [1] Without therapy, phlegmonous gastritis progresses to peritonitis and death. In the preantibiotic era mortality was as high as 92% [2]. However, mortality remained high even after antibiotics became available (64%) [3, 4]. Therefore, early recognition and treatment are mandatory.

&lt;a name="home"&gt;&lt;/a&gt;The role of IFN-gamma and IL-4 in gastric mucosa inflammation associated with Helicobacter heilmannii type 1 infection

Although Helicobacter heilmannii infection is less common than H. pylori infection in humans, it is considered to be of medical importance because of its association with gastritis, gastric ulcer, carcinoma, and mucosa-associated lymphoid tissue lymphoma of the stomach. However, there have been no studies evaluating the role of the Th cell response in H. heilmannii gastric infection. We evaluated the participation of pro-inflammatory and anti-inflammatory cytokines, IFN-gamma and IL-4, in H. heilmannii gastric infection in genetically IFN-gamma- or IL-4-deficient mice. The serum IFN-gamma and IL-4 concentrations were determined by ELISA. The gastric polymorphonuclear infiltrate was higher (P = 0.007) in H. heilmannii-positive than in H. heilmannii-negative wild-type (WT) C57BL/6 mice, whereas no significant inflammation was demonstrable in the stomach of H. heilmannii-positive IFN-gamma(-/-) C57BL/6 mice. The degree of gastric inflammatory cells, especially in oxyntic mucosa, was also higher (P = 0.007) in infected IL-4(-/-) than in WT BALB/c mice. Serum IFN-gamma levels were significantly higher in IL-4(-/-) than in WT BALB/c mice, independently of H. heilmannii-positive or -negative status. Although no difference in serum IFN-gamma levels was seen between H. heilmannii-positive (11.3 +/- 3.07 pg/mL, mean +/- SD) and -negative (11.07 +/- 3.5 pg/mL) WT BALB/c mice, in the group of IL-4(-/-) animals, the serum concentration of IFN-gamma was significantly higher in the infected ones (38.16 +/- 10.5 pg/mL, P = 0.04). In contrast, serum IL-4 levels were significantly decreased in H. heilmannii-positive (N = 10) WT BALB/c animals compared to the negative (N = 10) animals. In conclusion, H. heilmannii infection induces a predominantly Th1 immune response, with IFN-gamma playing a central role in gastric inflammation.

Helicobacter heilmannii infection: Clinical, endoscopic and histopathological features in Japanese patients

Gastric biopsy materials of 4074 consecutive Japanese patients undergoing esophagogastroduodenoscopy were reviewed, along with those of 15 patients with Helicobacter heilmannii infection (11, chronic gastritis; four, mucosa-associated lymphoid tissue (MALT) lymphoma). In four patients with H. heilmannii infection, the materials were examined by transmission electronmicroscopy. Urea breath test (three patients) and antibody test (five patients) were performed in patients with H. heilmannii infection. In two patients with MALT lymphoma, H. heilmannii was eradicated. The prevalence of H. heilmannii was 0.1% in the consecutive series. In chronic gastritis, the gastric mucosa was endoscopically normal (13.3%), had erythema (33.3%), or had erosions (53.3%); histologically, it showed no epithelial change, mild mononuclear cell infiltration, and slight and focal neutrophil infiltration; Helicobacter heilmannii was positive with anti-H. pylori antibody, and was detected in the mucous gel layer and in foveolae. In MALT lymphoma, the gastric mucosa was coarsely granular with enlarged mucosal folds without ulcers (two cases), with small ulcers (one case), or with multiple erosions (one case). Urea breath test and antibody test were both negative. Eradication of H. heilmannii resulted in remission of MALT lymphoma. Helicobacter heilmannii infection is therefore uncommon in Japanese adults, but is associated with chronic gastritis and gastric MALT lymphoma.

Helicobacter heilmannii infection in a child after successful eradication of Helicobacter pylori: case report and review of literature

An 11-year-old boy with Helicobacter pylori-associated duodenal ulcer was successfully treated with a combination of lansoprazole, amoxicillin, and clarithromycin. Endoscopy and gastric biopsies were repeated 2 and 12 months later, showing ulcer healing and eradication of H. pylori. However, a 3-year follow-up study demonstrated H. heilmannii in the antral mucosa based on its characteristic morphology and positive urease test and negative culture. The patient had no contact with domestic animals such as cats and dogs. A 7-day course with lansoprazole, amoxicillin, and clarithromycin was performed again, resulting in successful eradication of the organism. Pediatric cases with H. heilmannii infection reported are reviewed.