Potential Role of Biofilm Formation in the Development of Digestive Tract Cancer With Special Reference to Helicobacter pylori Infection (original) (raw)
Identification of Helicobacter pylori Biofilms in Human Gastric Mucosa
Journal of Gastrointestinal Surgery, 2006
The purpose of this study was to use endoscopically directed biopsies and scanning electron microscopy (SEM) to document the existence of Helicobacter pylori biofilms in human gastric mucosa. Patients underwent flexible esophagogastroduodenoscopies with three gastric mucosal biopsies. Rapid urease testing was performed to determine the presence or absence of H pylori. Urease-positive and urease-negative control specimens were imaged with SEM to obtain detailed images of gastric mucosa for the identification of biofilm colonies. Samples were obtained from patients who underwent esophagogastroduodenoscopies. Eleven were found to be H pylori positive and nine were H pylori negative. These were imaged at 5003 and 10003 with electron microscopy. Dense, mature biofilms were present and attached to the cell surface of H pylori-positive specimens and were absent in urease-negative controls. Photomicrographs were obtained. Biofilms are complex microbiological ecosystems where sessile bacteria surround themselves in a protective matrix. This lifestyle affords protection, allows for growth in hostile environments, and alters host physiology. Many have hypothesized that H pylori infections resulting in gastric ulcers may be a manifestation of biofilms. Our investigation is the first to photographically document the existence of H pylori biofilms on human gastric mucosa. This elucidation of the ecology and pathophysiology of the mucosa of the organism is important to our understanding of a potential mechanism of this organism's resistance to current therapy and how to better eradicate it in the future.
Helicobacter pylori induced gastric cancer
Gastric cancer is one of the most common cancer-related deaths worldwide. Helicobacter pylori has been recognized as one the most important etiologic agents in the development of gastric cancer. A number of virulence factors, that are utilized by this pathogen to establish and to maintain colonization of the stomach, have been investigated to date: adhesion proteins, urease, CagA, VacA, and outer membrane vesicleswhich all not only help the bacterium to maintain its gastric niche, but also to escape the damaging response from the immune system. Standard treatment protocols have been developed for eradication of this infection; however, the treatment failure and reinfection rates are still quite high, particularly, due to the formation of biofilms by this pathogen. Therefore, it might be reasonable to explore the strategies to combat biofilm formation in the stomach in order to improve the success rates of the conventional therapies and to possibly prevent the development of gastric cancer. This review will focus on the virulence factors that are employed by the pathogen, on its interaction with the host immune system, and on conventional treatment protocols, as well as on biosurfactant agents and natural supplements that can be possibly used for biofilm destruction in stomach.
Biofilm and Helicobacter pylori: from environment to human host
World journal of gastroenterology : WJG, 2014
Helicobacter pylori (H. pylori) is a Gram negative pathogen that selectively colonizes the human gastric epithelium. Over 50% of the world population is infected with H. pylori reaching up to 90% of infected individuals in developing countries. Nonetheless the increased impact upon public health care, its reservoir and the transmission pathway of the species has not been clearly established yet. Molecular studies allowed the detection of H. pylori in various aquatic environments, even forming biofilm in tap water distribution systems in several countries, suggesting a role of water as a possible reservoir of the pathogen. The persistence of human infection with H. pylori and the resistance of clinical isolates to commonly used antibiotics in eradication therapy have been related to the genetic variability of the species and its ability to develop biofilm, demonstrated both in vivo and in vitro experiments. Thus, during the last years, experimental work with this pathogen has been fo...
Biofilm Formation Capability of Clinical Helicobacter pylori Isolates on MKN-45 Cells
Jentashapir Journal of Cellular and Molecular Biology
Background: In vitro biofilm formation of H. pylori is demonstrated; however, its potential role in the persistent infection of the human stomach has not yet been addressed. Objectives: The aim of this study was to assess the biofilm formation of clinical H. pylori isolates on an epithelial cell line, a line that produces mucin. Methods: H. pylori isolates consisting of an efficient (19B) and a weak (4B) biofilm formation ability, were selected from screening of the clinical isolates. Their adhesion index was determined after 2h incubation with the semi-confluent monolayers of MKN-45 cells. Their biofilm formation was evaluated after 24 and 72 h incubation with MKN-45 cells using a modified adherence assay developed in this work. Production of biofilm was quantitatively assessed by CFU enumeration and qualitatively by the immunofluorescence, and scanning-electron-microscopic (SEM) methods. Due to the importance of mucin in the binding of H. pylori and biofilm formation, the binding ...
Journal of Gastrointestinal Surgery, 2006
Our purpose was to use endoscopically directed biopsies and scanning electron microscopy to quantify Helicobacter pylori biofilm density on the surface of human gastric mucosa in urease-positive and-negative patients. Participating patients underwent flexible esophagogastroduodenoscopies coupled with gastric mucosal biopsies. Rapid urease testing was performed on all specimens to determine the presence of H. pylori, followed by scanning electron microscopy to identify the existence of biofilms. Samples were then analyzed using Carnoy Image Analysis Software to determine percent biofilm coverage of the total surface area. These data were compared to control specimens that were urease negative. Of the patients who tested urease positive for H. pylori, the average percent of total surface area covered by biofilms was 97.3%. Those testing negative had an average surface area coverage of only 1.64%. These differences were determined to be statistically significant at the 0.0001 level. This study demonstrates that compared with controls, urease-positive specimens have significant biofilm formation, whereas urease-negative specimens have little to none. This was reflected in the significantly increased biofilm surface density in urease positive specimens compared with urease-negative controls.
Study of biofilm formation in C57Bl/6J mice by clinical isolates of Helicobacter pylori
Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association
Despite the significant number of studies on H. pylori pathogenesis, not much data has been published concerning its ability to form biofilm in the host stomach. This study aims to evaluate the potential of clinical isolates of H. pylori to form biofilm in C57BL/6J mice model. Two strains of H. pylori were selected from a collection of clinical isolates; one (19B), an efficient biofilm producer and the other (4B), with weak biofilm-forming ability. Mice infected through gastric avages were examined after one and two weeks. Colonization was determined by CFU and urease activity; the anti-H. pylori IgA was measured by ELISA, and chronic infections were evaluated by histopathology. Bacterial communities within mucosal sections were studied by immunofluorescence and scanning electron microscopy (SEM). Successful infection was obtained by both test strains. Strain 19B with higher ability to form biofilm in vitro also showed a higher colonization rate in the mice stomach one week after in...
Helicobacter pylori in promotion of gastric carcinogenesis
Digestive Diseases and Sciences, 1996
Gastric atrophy and intestinal metaplasia are considered the earliest phenotypic changes in the cascade of events leading from normal mucosa to intestinal-type gastric cancer, and epidemiologicai evidence links Helicobacter pylori to gastric epithelial malignancies. To evaluate any causal relationship between bacterial infection and atrophic metaplastic lesions, gastric pathology was histologically and histochemically evaluated in 267 consecutive, nonulcerous, untreated subjects, with attention given to the phenotypes of intestinal metaplasia.
Helicobacter pylori-coccoid forms and biofilm formation
FEMS Immunology & Medical Microbiology, 2009
Electron microscopic studies have shown that Helicobacter pylori occurs in three stages: spiral forms, coccoid forms and degenerative forms. The spiral forms are viable, culturable, virulent and can colonize experimental animals and induce inflammation. The coccoid forms may also be viable but are nonculturable, less virulent and are less likely to colonize and induce inflammation in experimental animals than the spiral forms. The degenerative forms are pyknotic, nonculturable, coccoid forms of dead H. pylori. These forms cannot be cultured and the cell membrane has disintegrated but gene material can be detected by PCR in water supplies. There is no substantial evidence for viable H. pylori persisting in water supplies. Epidemiological studies suggest that environmental water is a risk factor for H. pylori infection when compared with tap water, and formation of H. pylori biofilm cannot be excluded. Helicobacter pylori does not seem to take part in biofilm formation in the oral cavity even though the bacterium may be detected.
Biofilm Formation and Antibiotic Resistance Phenotype of Helicobacter pylori Clinical Isolates
Toxins
We evaluated biofilm formation of clinical Helicobacter pylori isolates from Indonesia and its relation to antibiotic resistance. We determined the minimum inhibition concentration (MIC) of amoxicillin, clarithromycin, levofloxacin, metronidazole and tetracycline by the Etest to measure the planktonic susceptibility of 101 H. pylori strains. Biofilms were quantified by the crystal violet method. The minimum biofilm eradication concentration (MBEC) was obtained by measuring the survival of bacteria in a biofilm after exposure to antibiotics. The majority of the strains formed a biofilm (93.1% (94/101)), including weak (75.5%) and strong (24.5%) biofilm-formers. Planktonic resistant and sensitive strains produced relatively equal amounts of biofilms. The resistance proportion, shown by the MBEC measurement, was higher in the strong biofilm group for all antibiotics compared to the weak biofilm group, especially for clarithromycin (p = 0.002). Several cases showed sensitivity by the MI...