scholarly journals Galectin-2 Has Bactericidal Effects against Helicobacter pylori in a β-galactoside-Dependent Manner

2020 ◽  
Vol 21 (8) ◽  
pp. 2697 ◽  
Author(s):  
Takaharu Sasaki ◽  
Rei Saito ◽  
Midori Oyama ◽  
Tomoharu Takeuchi ◽  
Toru Tanaka ◽  
...  

Helicobacter pylori is associated with the onset of gastritis, peptic ulcers, and gastric cancer. Galectins are a family of β-galactoside-binding proteins involved in diverse biological phenomena. Galectin-2 (Gal-2), a member of the galectin family, is predominantly expressed in the gastrointestinal tract. Although some galectin family proteins are involved in immunoreaction, the role of Gal-2 against H. pylori infection remains unclear. In this study, the effects of Gal-2 on H. pylori morphology and survival were examined. Gal-2 induced H. pylori aggregation depending on β-galactoside and demonstrated a bactericidal effect. Immunohistochemical staining of the gastric tissue indicated that Gal-2 existed in the gastric mucus, as well as mucosa. These results suggested that Gal-2 plays a role in innate immunity against H. pylori infection in gastric mucus.

2021 ◽  
Vol 8 (1) ◽  
pp. 160-165
Author(s):  
Masaaki Minami ◽  
Takafumi Ando ◽  
Hidemi Goto ◽  
Michio Ohta

Mupirocin (MUP) is an effective antibiotic against MRSA. Its bactericidal effect is stable under acid condition. By validating its antibacterial effect of Helicobacter pylori, we try to clarify MUP effect on H. pylori. The present study was conducted to investigate the effect of MUP on clarithromycin (CLR) / metronidazole (MNZ) -resistant and -susceptible strains of H. pylori, the time-kill effect of MUP, and the post antibiotic effect (PAE). We investigated the minimal inhibitory concentration (MIC) and the minimal bactericidal effect (MBC) of MUP against 140 H. pylori, which include clinical strains, ATCC43504, 26695 and J99. Ten of them were CLR -resistant strains and 3 were MNZ-resistant strains. The MIC90 and MBC of MUP on all 140 strains is 0.064 μg / ml, and 0.1 μg / ml, respectively. There were no differences of MUP effect between susceptible and resistant strains either for CLR or MNZ. Time-kill curve test and PAE test of MUP on ATCC43504 were performed. By adding MUP, time-kill curve showed that bacterial quantities decreased in dose and time-dependent manner. No viable colony was found after 12-hour culture with 0.1 μg / ml MUP. The value of PAE is 12. MUP is a potential effective antibiotic for H. pylori even those for CLR / MNZ -resistant strains.


Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 109
Author(s):  
María Guerra-Valle ◽  
Patricio Orellana-Palma ◽  
Guillermo Petzold

Helicobacter pylori (H. pylori) infection affects more than half of the world’s population, and thus, about 10 to 20% of people with H. pylori suffer from peptic ulcers, which may ultimately lead to gastric cancer. The increase in antibiotic resistance and susceptibility has encouraged the search for new alternative therapies to eradicate this pathogen. Several plant species are essential sources of polyphenols, and these bioactive compounds have demonstrated health-promoting properties, such as the gut microbiota stimulation, inflammation reduction, and bactericidal effect. Therefore, this review aims to discuss the potential effect of plant-based polyphenols against H. pylori and their role in the gut microbiota improvement.


2021 ◽  
Vol 9 (3) ◽  
pp. 193-204
Author(s):  
Serah Funke Ige ◽  
◽  
Bolade S. Olateju ◽  
Victor A. Oladipupo ◽  
Adedayo T. Adekola ◽  
...  

Peptic ulcers are described as acid-induced lesions found in the stomach and duodenum caused bythe imbalance between the defending factors of the mucosa and the attacking factors such ashydrochloric acid in gastric juice, with Helicobacter Pylori (H. Pylori) and Non-Steroidal Anti-Inflammatory Drugs NSAIDs. They exhibit seasonal patterns in their occurrence, with higheroccurrence in winter and spring and a low occurrence in summer. Temperature plays a major role intheir occurrence, some of which have resulted in increased morbidity in some number of diseases,such as gastrointestinal bleeding, caused by an increase in air pressure, dry air (relative humidity)occurring from cold air, and also its actions on the protective effect helicobacter pylori in the humanbody. Their actions excite the adrenal gland marrow and the sympathetic nerve, causing rapidsecretion of adrenaline and non-adrenaline, angiotensin II and endothelin, resulting in damage tothe mucosa epithelial, caused by the contraction effect of the adrenal agents on the duodenalmucosa and blood vessel. It causes low expression of Epidermal Growth Factor Receptor (EGFR),Epidermal Growth Factor (EGF), Heat Shock Protein (HSP) 70, Occludin, Nitric Oxide Synthase(NOS), in the gastric mucosa, in extremely cold temperature than those in extremely hottemperature, increasing the gastric acid secretion in extremely cold temperature than in extremelyhot temperature. Therefore, this review aims to give general insight into the role of low temperaturein peptic ulcer development and further consideration in the treatment of peptic ulcer diseases.


2001 ◽  
Vol 45 (6) ◽  
pp. 1700-1704 ◽  
Author(s):  
Johan Bylund ◽  
Thierry Christophe ◽  
Francois Boulay ◽  
Thomas Nyström ◽  
Anna Karlsson ◽  
...  

ABSTRACT Helicobacter pylori, the bacterial pathogen associated with gastritis and peptic ulcers, is highly successful in establishing infection in the human gastric mucosa, a process typically associated with massive infiltration of inflammatory cells. Colonization of the mucosa is suggested to be facilitated by H. pylori-produced cecropin-like peptides with antibacterial properties, giving the microbe a competitive advantage over other bacteria. We show that a cecropin-like antibacterial peptide from H. pylori, Hp(2-20), not only has a potent bactericidal effect but also induces proinflammatory activities in human neutrophils, e.g., upregulation of integrins (Mac-1), induction of chemotaxis, and activation of the oxygen radical producing NADPH-oxidase. Furthermore, we show that these effects are mediated through binding of Hp(2-20) to the promiscuous, G-protein-linked lipoxin A4 receptor–formyl peptide-like receptor 1.


2020 ◽  
Vol 21 (5) ◽  
pp. 1801
Author(s):  
Weronika Gonciarz ◽  
Agnieszka Krupa ◽  
Magdalena Chmiela

Interleukin (IL)-33 is a proinflammatory mediator that alerts the host immune system to disorders in tissue homeostasis. Aim. To understand the role of IL-33 in modulating gastric tissue cell growth affected by Helicobacter pylori (H. pylori). Methods. IL-33 production in guinea pigs (Caviae porcellus) experimentally infected with H. pylori was evaluated by ELISA or immunohistochemical staining. The proregenerative activity of IL-33 was evaluated using gastric epithelial cells and fibroblasts that were naive or transfected with IL-33 siRNA exposed to H. pylori glycine acid extract antigenic complex (GE), as well as by measuring cell migration, proliferation, metabolic activity and apoptosis. Animals infected by H. pylori responded with increased production of IL-33. Also, cells treated in vitro with GE released more IL-33 than cells that were unstimulated. Silencing IL-33 in cells resulted in downregulation of metabolic activity, adhesion, migration and proliferation, especially after treatment with H. pylori GE, as well as upregulation of cells apoptosis associated with caspase 3 increase and Bcl-xL decrease, suggesting proregenerative activity of IL-33. Interestingly, upregulation of cell proliferation by IL-33 was Erk independent. Our results indicate that IL-33 may protect gastric tissue from loss of homeostasis caused by deleterious effects of H. pylori components and the inflammatory response developed during infection.


2005 ◽  
Vol 19 (1) ◽  
pp. 37-41
Author(s):  
Mohammed S Al-Marhoon ◽  
Sheila Nunn ◽  
Roger W Soames

BACKGROUND AND AIMS: Infection with cytotoxin-associated gene A (cagA) Helicobacter pylori is associated with severe gastric diseases. Previous studies in humans have reported a decreased gastric hydrophobicity with H pylori infection. The aim of the present study was to differentiate between the effect of cagA+ and cagA- strains on gastric mucus hydrophobicity.METHODS: One hundred patients without peptic ulcers and not on medication were randomly recruited from endoscopy clinics; each patient had six biopsies. Contact angle measurements were performed using a goniometer assisted by computer software. H pylori status was assessed by histology, Campylobacter-like organism test and culture, and cagA+ status was determined by polymerase chain reaction.RESULTS: In age- and sex-matched patients, there was no significant difference (P=0.27) in contact angle between H pylori-positive (61±2.8°) and H pylori-negative patients (65.5±3.0°). There was also no significant difference (P=0.36) in contact angle among H pylori-negative, cagA- and cagA+ patients (65.5±3.0°, 58.6±3.6° and 63.4±4.9°, respectively). However, a trend of increased mean contact angles in cagA+ compared with cagA- and H pylori-negative patients was observed in patients 50 years and younger (68.3±8.3°, 61.1±6.1° and 63.6±2.2°, respectively; P=0.70) and in patients without atrophy (71.1±8°, 59.6±4° and 66±2°, respectively; P=0.30). In addition, there was no significant correlation between contact angles and patient age (r=0.104, P=0.306).CONCLUSIONS: The present study shows that H pylori infection and the chronological age have no effect on the gastric mucus hydrophobicity, but it highlights a trend of increased mucus hydrophobicity with cagA+ infection that needs to be supported by future studies.


2020 ◽  
Vol 7 (7) ◽  
pp. 2097
Author(s):  
Jehan Sabah Hasan ◽  
Mohammed Ahmed Alshami

Background: Helicobacter pylori is a gastric organism was first observed more than 100 years ago. It may cause chronic gastritis, peptic ulcers and gastric adenocarcinoma and lymphoma. It can produce some extragastric disorders including preeclampsia. This study aimed to focus on the importance of H. pylori and its relationship with preeclampsia and gastric illnesses in pregnant patients.Methods: This study includeed 100 pregnant women, half of them were healthy and the other half with preeclampsia. Patients with chronic medical illnesses were excluded. Data was collected and laboratory investigations were done including that for H. pylori. Oesophagogastroduodenoscopy then was done 6 weeks post-delivery or termination of pregnancy for symptomatic H. pylori positive women.Results: 50% of the total number were healthy, 17% had mild preeclampsia, 33% suffering from severe preeclampsia. Seropositivity for H. pylori is significantly higher in preeclampsia and significantly related to severity of preeclampsia and complications of pregnancy. Positive H. pylori test in stool was seen in (45%) of total number of patients. Epigastric pain persist in 41 (91%) of patients with positive H. pylori test in stool. Gastritis, duodenal ulcer, and gastric ulcer were found in 85.3%, 12.1% and 2.4% of symptomatic patients respectively.Conclusions: Significant correlation between Helicobacter pylori seropositivity and preeclampsia may indicate the benefit of using this parameter in the prediction and management of preeclampsia and its severity. H. pylori infection plays an important role in gastric pathologies in pregnant women that can be dealt with or may be prevented more efficiently in future. 


Background and aim: Helicobacter pylori (H. pylori) is an incriminated pathogen causing diseases in both animals and humans and considered a zoonotic pathogen. H. pylori infection is considered a cause of gastric cancer, which rests a significant health care challenge. This study analyzes the expression pattern of matrix metalloprotein 2 (MMP-2) in patients with Helicobacter pylori-associated gastritis and the effect of H. pylori on gastric cancer stem cells, as well as study the role of helicon bacteriosis in dog in transmission of H. pylori infection to human. Materials and methods: Fifty-five of each sample (gastric biopsy, blood and stool) were collected from patients suffering from dyspepsia, chronic vomiting and perforated peptic ulcers and also from apparent healthy dogs. The investigation detected H. pylori by serological and histopathological examination. Biopsies were stored in physiological saline for identification of H. pylori by conventional time PCR. MMP-2 and Gastric cancer stem cells were then identified by immunohistochemistry. Results: Serological identification for H. pylori Antigen and Antibodies revealed (63% human, 50% dogs) and (87% human, 90% dogs) respectively were positive. Genotyping of H. pylori based on 16S rRNA gene showed 54.5% of human and 35% of dogs were positive. Immunohistochemistry revealed strong expression of CD44 in H. pylori- associated gastric cancer cases, MMP-2 expression was observed in all neoplastic lesions associated with H. pylori infection. Conclusion: H. pylori infection affects gastric mucosa and induces changes in gastric stem cells altering their differentiation and increased expression of MMP’s and CD44with a resultant potentiation of oncogenic alteration. In addition the up-regulation of both markers could be an instrumental to interpret the origination of gastric cancer.


Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 982
Author(s):  
Xiaoyan Peng ◽  
Rongguang Zhang ◽  
Chen Wang ◽  
Feiyan Yu ◽  
Mingyang Yu ◽  
...  

Current studies indicate that the anti-H. pylori protective efficacy of oral vaccines to a large extent depends on using mucosal adjuvants like E. coli heat-lable enterotoxin B unit (LtB). However, the mechanism by which Th17/Th1-driven cellular immunity kills H. pylori and the role of LtB remains unclear. Here, two L. lactis strains, expressing H. pylori NapA and LtB, respectively, were orally administrated to mice. As observed, the administration of LtB significantly enhanced the fecal SIgA level and decreased gastric H. pylori colonization, but also markedly aggravated gastric inflammatory injury. Both NapA group and NapA+LtB group had elevated splenocyte production of IL-8, IL-10, IL-12, IL-17, IL-23 and INF-γ. Notably, gastric leukocytes’ migration or leakage into the mucus was observed more frequently in NapA+LtB group than in NapA group. This report is the first that discusses how LtB enhances vaccine-induced anti-H. pylori efficacy by aggravating gastric injury and leukocytes’ movement into the mucus layer. Significantly, it brings up a novel explanation for the mechanism underlying mucosal cellular immunity destroying the non-invasive pathogens. More importantly, the findings suggest the necessity to further evaluate LtB’s potential hazards to humans before extending its applications. Thus, this report can provide considerable impact on the fields of mucosal immunology and vaccinology.


Pathogens ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 331
Author(s):  
Montserrat Palau ◽  
Núria Piqué ◽  
M. José Ramírez-Lázaro ◽  
Sergio Lario ◽  
Xavier Calvet ◽  
...  

Helicobacter pylori is a common pathogen associated with several severe digestive diseases. Although multiple virulence factors have been described, it is still unclear the role of virulence factors on H. pylori pathogenesis and disease progression. Whole genome sequencing could help to find genetic markers of virulence strains. In this work, we analyzed three complete genomes from isolates obtained at the same point in time from a stomach of a patient with adenocarcinoma, using multiple available bioinformatics tools. The genome analysis of the strains B508A-S1, B508A-T2A and B508A-T4 revealed that they were cagA, babA and sabB/hopO negative. The differences among the three genomes were mainly related to outer membrane proteins, methylases, restriction modification systems and flagellar biosynthesis proteins. The strain B508A-T2A was the only one presenting the genotype vacA s1, and had the most distinct genome as it exhibited fewer shared genes, higher number of unique genes, and more polymorphisms were found in this genome. With all the accumulated information, no significant differences were found among the isolates regarding virulence and origin of the isolates. Nevertheless, some B508A-T2A genome characteristics could be linked to the pathogenicity of H. pylori.


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