Helicobacter pylori (H. pylori), a long term colonizer of human stomach is known to infect a half of mankind. Gastric and duodenal ulcer, gastric adenocarcinoma and MALT lymphoma develop in a subset of infected individuals. Pathogenesis of H. pylori infection is based on the long-term host to bacterial interaction and affected by the virulence factors of the bacterium, environmental and host factors (age, sex, blood type). Mucosal inflammation is the basic principle mechanism underlying the disease development in which tissue destruction may be initiated and maintained by both the bacterial toxins (CagA, VacA, LPS) and immune responses by the host. Immune evasion with bacterial modulation of host response affects the long-term host colonization. Colonization is also affected by urease and/or motility of the bacterium, presence of lipopolysaccharide (LPS) and various bacterial enzymes. Gastric mucosal atrophy and intestinal metaplasia can develop during the course of H. pylori infection predisposing to carcinogenesis. Host cytokine gene polymorphism would be the one explanation for host susceptibility to peptic ulcer or gastric cancer. Investigation into the pathogenesis of H. pylori related diseases could provide an answer to the impact of chronic host to microbial interaction resulting human diseases.
Gastrointestinal Diseases ; Helicobacter Infections/microbiology/*physiopathology ; *Helicobacter pylori/physiology ; Humans

Helicobacter pylori (H. pylori) undergoes decades long colonization of the gastric mucosa of half the population in the world to produce acute and chronic gastritis at the beginning of infection, progressing to more severe disorders, including peptic ulcer disease and gastric cancer. Prolonged carriage of H. pylori is the most crucial factor for the pathogenesis of gastric maladies. Bacterial persistence in the gastric mucosa depends on bacterial factors as well as host factors. Herein, the host and bacterial components responsible for the incipient stages of H. pylori infection are reviewed and discussed. Bacterial adhesion and adaptation is presented to explain the persistence of H. pylori colonization in the gastric mucosa, in which bacterial evasion of host defense systems and genomic diversity are included.
Gastric Mucosa/*microbiology ; Gastritis/*microbiology/pathology ; Helicobacter Infections/*microbiology ; Helicobacter pylori/*physiology ; Humans ; Stomach Neoplasms/pathology

DNA Methylation ; Helicobacter Infections ; complications ; Helicobacter pylori ; Humans ; Stomach Neoplasms ; etiology ; genetics ; Telomerase ; physiology

OBJECTIVETo isolate the wild-type virulent phage of Helicobacter pylori (Hp) and simulate the treatments in vitro to investigate the methods for oral Hp-assisted penetration of the phage through the gastric barrier and offspring phage release for infection and treatment of gastrointestinal Hp.

METHODSThe Hp strain was cultured with the candle cylinder method and the virulent phage was isolated by single plate or double plate experiment. A simulated gastric juice was applied and the bactericidal effect of the phage was tested with double flats experiment.

RESULTSAfter a 1.5-h treatment in simulated gastric juice, the orally derived Hp-borne phage was still capable of forming plaques while the control phage was not.

CONCLUSIONThe oral Hp can help the phage resist the gastric juice and then infect the gastrointestinal Hp.

Bacteriophages ; isolation & purification ; physiology ; Gastrointestinal Tract ; microbiology ; Helicobacter Infections ; therapy ; Helicobacter pylori ; virology ; Humans ; Virulence

Helicobacter pylori (H. pylori) is the causative agent of chronic gastritis and peptic ulcer diseases and is an important risk factor for the development functional dyspepsia, peptic ulceration, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma. H. pylori has very high rates of infection in human populations, and it is estimated that over 50% of the world population is infected. Recently, certain extra-gastric manifestations, linked to H. pylori infection, have been widely investigated. Noteworthy, a growing body of evidences supports an association between H. pylori infection with lung cancer. The present review intend to highlight not only the most recent evidences supporting this association, but also some missed points, which must be considered to validate this emerging association.
Helicobacter Infections ; complications ; Helicobacter pylori ; physiology ; Humans ; Lung Neoplasms ; complications ; microbiology

OBJECTIVETo assess the prevalence rate of Helicobacter pylori (H. pylori) in blood serum, its affecting factors and isoforms (CagA,VacA )infection in the elderly people in Beijing.

METHODS2006 residents were investigated through household questionnaire in different areas of Beijing (urban, suburban and mountainous district), who were older than 60 years old. Serum H. pylori CagA, VacA and Ureas antibody was detected by immunoblotting.

RESULTSThe total H. pylori infection rate was 83.4% and the infectious rate of I form pathogenic H. pylori was 56.0%. The incidence rate in urban or suburban district was higher than that of in mountainous district (P < 0.001). I form H. pylori infection rate in people with heavy labor or young elderly were higher than that of intelegent work or older elderly (P < 0.05 ). I form H. pylori infection rate in people of low diet was higher than that of high protein diet (P < 0.001).

CONCLUSIONThe rate of H. pylori infection in blood serum was high among the elderly people in Beijing with most of it belonged to type I . However, significant differences were noticed on the distribution of isoforms in different age groups, areas, professions and diet habit.

Age Distribution ; Aged ; China ; epidemiology ; Diet ; Female ; Helicobacter Infections ; blood ; epidemiology ; Helicobacter pylori ; classification ; physiology ; Humans ; Male ; Occupations ; Seroepidemiologic Studies

BACKGROUND/AIMS: Gastric juice plays a crucial role in the physiology of the stomach. The aim of this study is to evaluate associations among the pH of gastric juice, atrophic gastritis (AG), intestinal metaplasia (IM), pepsinogen, and Helicobacter pylori infection. METHODS: Gastric biopsies and juice were collected from 46 subjects who underwent endoscopies at Seoul National University Bundang Hospital between November 2011 and March 2013. H. pylori, AG and IM were evaluated, and pepsinogen I or II, I/II ratio, and interleukin (IL)-1β levels were measured. RESULTS: The mean pH of gastric juice was higher in the H. pylori-positive group (n=17) than that in the H. pylori-negative group (n=29) (4.54 vs 2.46, p=0.002). When patients were divided into pH < 3 (n=28) and pH ≥3 (n=18) groups, H. pylori was lower in the pH < 3 group (21.4%) than in the pH ≥3 group (61.1%) (p=0.007). The pH ≥3 group demonstrated AG and IM more frequently than the pH < 3 group in the body (p=0.047 and p=0.051, respectively) but not in the antrum. There were no differences in pepsinogen I or II, I/II ratio, and IL-1β levels between the two groups. CONCLUSIONS: There is a relationship between chronic H. pylori infection and gastric juice pH ≥3, which may originate from AG and IM in the body.
Biopsy ; Gastric Juice* ; Gastritis ; Gastritis, Atrophic* ; Helicobacter pylori* ; Helicobacter* ; Humans ; Hydrogen-Ion Concentration* ; Interleukins ; Metaplasia* ; Pepsinogen A ; Physiology ; Seoul ; Stomach

OBJECTIVE: To observe the therapeutic effect of Bacillus acidi lactici on Helicobacter Pylori (Hp) infectious gastritis in Balb/c mouse model so as to explore a possible non-antibiotic treatment for Hp. METHODS: To establish a Balb/c mouse model with Hp infectious gastritis through inoculation of mankind Hp,32 Balb/c mice infected by Hp were randomly divided into 4 groups:Group 1(PPI trigeminy treatment group),Group 2 (Bacillus acidi lactici CL22 treatment group),Group 3 (Bacillus acidi lactici CL24 treatment group),and Group 4 (normal saline control group). Intragastric administration was given continuously for 10 days. Another 8 normal mice were chosen as Group 5(blank control group). All mice were killed after 4 weeks since last intragastric administration. Hp was detected by rapid urease test,Giemsa dying, and bacterial culture,and histopathologic changes in the gastric mucosa of mice were determined by H-E staining. RESULTS: There were significant differences in pathohistologic scores in sinus ventriculi among the 5 groups (F = 7.932, P = 0.000). The scores in Group 1, Group 2, Group 3, and Group 5 were obviously lower than those in Group 4 (P < 0.05), but there were not significant differences among Group 1, 2, and 5 (P>0.05). The pathohistologic score in Group 3 was obviously higher than that in Group 5 (P <0.05). There were significant differences in pathohistologic scores in corpus ventriculi among the 5 groups (F = 6.241, P = 0.001). The scores in Group 1,Group 2,Group 3,and Group 5 were obviously lower than those in Group 4(P <0.05), but there were not significant differences among Group 1, 2, 3,and 5 (P>0.05). There was significant difference in Hp eradication rates in sinus ventriculi among the 5 groups (chi2 = 16.923, P=0.002). The Hp eradication rates in Group 1 and 2 were obviously lower than those in Group 4 (P <0.05), but there was not significant difference between Group 1 and Group 2, Group 3 and Group 4 (P>0.05). There also were significant differences in Hp eradication rate in corpus ventriculi among the 5 groups (chi2 = 14.295, P=0.006). Of them, Group 1 and Group 2 were higher than Group 4 (P <0.05), but there were not obviously differences between Group 1 and 2,Group 3 and 4 (P>0.05). CONCLUSION Bacillus acidi lactici strain CL22 can effectively inhibit and eradicate Hp in Balb/c mouse model with Hp infectious gastritis in vivo. The therapeutic effect of Bacillus acidi lactici strain CL22 is equal to PPI + antibiotics and could be another choice of nonjantibiotic treatment for Hp.
Animals ; Antibiosis ; physiology ; Female ; Gastritis ; microbiology ; Helicobacter Infections ; microbiology ; therapy ; Helicobacter pylori ; Lactic Acid ; biosynthesis ; chemistry ; Lactobacillus ; metabolism ; physiology ; Male ; Mice ; Mice, Inbred BALB C ; Random Allocation

Animal ; Ascorbic Acid/metabolism ; Helicobacter Infections/*prevention & control ; Helicobacter pylori/*physiology ; Human ; Nitroso Compounds/metabolism ; Stomach Neoplasms/*microbiology ; Support, Non-U.S. Gov't

INTRODUCTIONHelicobacter pylori has been recognised as a major cause of gastroduodenal diseases, including gastric and duodenal ulcers with faeco-oral, oro-oral and gastro-oral transmission occurring. With the close personal contact inherent in patient care, health care workers may be at an increased risk of acquiring H. pylori and subsequent development of associated conditions. The objective of this review was to review the transmission and the occupational risk for health care workers.

METHODSA literature search was performed using Pubmed (January 1990 to May 2001). Relevant key words were used and additional manual searches were made using the reference lists from the selected articles to retrieve other papers relevant to the topic.

RESULTSCurrent knowledge implies various pathways of agent transmission, favouring person-to-person mode of transmission early in life. Faeco-oral, oro-oral and gastro-oral transmissions are proposed and may be of different relevance among various populations. As for health care workers, after elimination of the methodological weak studies, the risk seems to be increased in gastroenterologists, endoscopy staff and intensive care nurses. Results in other groups are conflicting.

CONCLUSIONSH. pylori infection is an occupational risk in some groups of health care workers. Studies are needed to elucidate the risk in other occupational groups.

Helicobacter Infections ; epidemiology ; microbiology ; transmission ; Helicobacter pylori ; physiology ; Humans ; Infectious Disease Transmission, Patient-to-Professional ; Medical Staff ; Occupational Diseases ; epidemiology ; microbiology ; Risk Factors