• Helicobacter pylori
• duodenal ulcer
• epidemiology
• gastric cancer
• gastritis
• virulence

• Animals
• Humans
• Bacterial Proteins/metabolism
• Gastritis/microbiology
• Helicobacter Infections/microbiology
• Helicobacter pylori/metabolism
• Helicobacter pylori/pathogenicity
• Host-Pathogen Interactions
• Persistent Infection/microbiology
• Stomach Neoplasms/microbiology
• Virulence
• Virulence Factors/metabolism

• Helicobacter pylori
• CagA
• Endodontics
• HtrA
• Root canal
• VacA

• Humans
• Helicobacter pylori/genetics
• Helicobacter pylori/physiology
• Tooth, Deciduous/microbiology
• Child
• Dental Pulp Cavity/microbiology
• Phylogeny
• Child, Preschool
• Female

• 953000-016 Deutsche Gesellschaft für Zahn-, Mund- und Kieferheilkunde
• Friedrich-Alexander-Universität Erlangen-Nürnberg (1041)

• Helicobacter pylori
• alternative therapies
• antibiotic resistance
• disease transmission
• infection control

• extracellular vesicles
• gastric Candida
• gastric colonization
• intracellular H. pylori
• oral Candida

• Helicobacter pylori/genetics
• Helicobacter pylori/physiology
• Helicobacter pylori/isolation & purification
• Humans
• Gastric Mucosa/microbiology
• Helicobacter Infections/microbiology
• Yeasts/genetics
• Yeasts/isolation & purification
• Yeasts/classification
• Yeasts/metabolism
• Female
• Male
• Adult
• Middle Aged
• Mouth/microbiology
• Biopsy
• Aged
• Immunohistochemistry

• This study was funded by the research council of Digestive Disease Research Institute, Tehran University of Medical Sciences, Iran (96043737026).

• Antibacterial
• Antibiotic-free
• MAXPOWER Biological Antibacterial Liquid
• Oral Helicobacter pylori
• Randomized controlled trials

• Helicobacter pylori/drug effects
• Helicobacter pylori/genetics
• Humans
• Helicobacter Infections/drug therapy
• Helicobacter Infections/microbiology
• Anti-Bacterial Agents/pharmacology
• Animals
• Mice
• Male
• Female
• Middle Aged
• Adult
• Microbial Sensitivity Tests

• YC2023-B102 Nanchang University Graduate Student Innovation Fund
• 23QA1412000 Shanghai Rising-Star Programand
• 2021-ZX-12 the Strategic Consulting Research Project of Chinese Academy of Engineering
• 2019SY001 the Project of Shanghai Municipal Health Commission
• 19MC1910200 Shanghai Clinical Medical Research Center for Digestive Diseases Project
• 21XD14049 Shanghai Outstanding Academic Leaders Program

• paediatric research
• experimental models of disease
• microbiome

• Animals
• Macaca mulatta/microbiology
• Lung/microbiology
• Helicobacter Infections/microbiology
• Helicobacter pylori/genetics
• Mouth/microbiology
• Microbiota
• RNA, Ribosomal, 16S/genetics
• Male
• Disease Models, Animal

• P51OD011107 NIH HHS
• R56AI091893 NIH HHS
• R56 AI091893 NIAID NIH HHS
• R01 AI138553 NIAID NIH HHS
• R01AI138553 NIH HHS
• P51 OD011107 NIH HHS
• National Institutes of Health

• P51 OD011107 NIH HHS
• R01 AI138553 NIAID NIH HHS
• R56 AI091893 NIAID NIH HHS

• GASTRIC CANCER
• GASTRIC PRE-CANCER
• HELICOBACTER PYLORI - EPIDEMIOLOGY
• HELICOBACTER PYLORI - GASTRITIS
• HELICOBACTER PYLORI INFECTION

• Child
• Adult
• Adolescent
• Humans
• Helicobacter pylori
• Helicobacter Infections/epidemiology
• Helicobacter Infections/prevention & control
• Family
• Risk Factors
• China/epidemiology
• Epidemiologic Studies
• Prevalence

• Project of Shanghai Municipal Health Commission
• National Clinical Research Center for Digestive Diseases
• Program of Shanghai Academic Research Leader
• Henan Provincial Government—Health and Family Planning Commission Science Research Innovative Talents Project
• National Natural Science Foundation of China
• Henan Provincial Government-Health and Family Planning Commission
• Program of National Key Research & Development

• Humans
• Helicobacter Infections/complications
• Helicobacter Infections/epidemiology
• Helicobacter pylori
• Stomach Neoplasms/microbiology
• Stomach Neoplasms/prevention & control
• Gastritis/complications
• Gastritis/diagnosis
• Gastritis/epidemiology
• Anti-Bacterial Agents/pharmacology
• Anti-Bacterial Agents/therapeutic use

• P01 CA116087 NCI NIH HHS
• P30 DK058404 NIDDK NIH HHS
• R01 CA077955 NCI NIH HHS
• R01 DK058587 NIDDK NIH HHS

• helicobacter pylori
• fecal-oral route
• infection transmission
• oral-oral route

• Helicobacter pylori
• Vietnam
• consensus
• diagnosis
• eradication
• guidelines
• management

Molecular diagnosis of helicobacters by PCR is simpler, more accurate, and feasible compared to other diagnostic methods. Validity and accuracy are highly dependent on the PCR primer design, diffusion time, and mutation rate of helicobacters. This study aimed to design 16srRNA -specific primers for Helicobacter spp. and H. pylori. Application of comparative statistical analysis of the diagnostic utility of the most available 16srRNA genus-specific primers. The new primers were designed using bioinformatics tools (MAFFT MSA and Gblocks command line). A comparative study was applied on nine genus-specific 16srRNA primers in comparison to the ConsH using in silico and laboratory evaluation. The results demonstrated that the best specificity and sensitivity of the primers designed for this study compared to other primers. The comparative study revealed that the heminested outer/inner primers were the worst. Although H276, 16srRNA(a), HeliS/Heli-nest, and Hcom had acceptable diagnostic utility, false positive and false negative results were obtained. Specificity testing on clinical samples indicated a surprising result; that H. pylori was not the sole enemy that we were looking for, but the Non-Helicobacter pylori Helicobacters should be considered as a real risk prognostic for gastric diseases, consequently, a specific diagnosis and treatment should be developed. This study concluded that our designed primers were the most specific and sensitive in comparison with other primers. In addition, in silico evaluation is not accurate enough for primer assessment and that the laboratory evaluation is mandatory.

• 13C-urea breath test
• gastric cancer
• helicobacter pylori
• helicobacter pylori - gastritis
• mucosal infection

• Adolescent
• Adult
• Aged
• Child
• Child, Preschool
• China
• Consensus
• Delphi Technique
• Family Health
• Helicobacter Infections/diagnosis
• Helicobacter Infections/prevention & control
• Helicobacter Infections/transmission
• Helicobacter pylori
• Humans
• Infant
• Infection Control/organization & administration
• Middle Aged
• Young Adult

• Africa
• Diagnosis
• Guideline
• Helicobacter pylori
• Treatment

• Helicobacter pylori
• Japan
• adolescents
• developmental disorders
• special needs schools

• 13C-urea breath test
• Children
• Gastrointestinal system
• Health sciences
• Helicobacter pylori
• Infection
• Infectious disease
• Jordan
• Laboratory medicine
• Pediatrics

Helicobacter pylori typically colonizes the human stomach, but it can occasionally be detected in the oral cavity of infected persons. Clinical outcome as a result of gastric colonization depends on presence of the pathogenicity island cagPAI that encodes a type-IV secretion system (T4SS) for translocation of the effector protein CagA and ADP-heptose. Upon injection into target cells, CagA is phosphorylated, which can be demonstrated by in vitro infection of the gastric epithelial cell line AGS, resulting in cell elongation. Here we investigated whether H. pylori can exert these responses during interaction with cells from the oral epithelium. To this purpose, three oral epithelial cell lines, HN, CAL-27 and BHY, were infected with various virulent wild-type H. pylori strains, and CagA delivery and ADP-heptose-mediated pro-inflammatory responses were monitored.

All three oral cell lines were resistant to elongation upon infection, despite similar bacterial binding capabilities. Moreover, T4SS-dependent CagA injection was absent. Resistance to CagA delivery was shown to be due to absence of CEACAM expression in these cell lines, while these surface molecules have recently been recognized as H. pylori T4SS receptors. Lack of CEACAM expression in HN, CAL-27 and BHY cells was overcome by genetic introduction of either CEACAM1, CEACAM5, or CEACAM6, which in each of the cell lines was proven sufficient to facilitate CagA delivery and phosphorylation upon H. pylori infection to levels similar to those observed with the gastric AGS cells. Pro-inflammatory responses, as measured by interleukin-8 ELISA, were induced to high levels in each cell line and CEACAM-independent.

These results show that lack of CEACAM receptors on the surface of the oral epithelial cells was responsible for resistance to H. pylori CagA-dependent pathogenic activities, and confirms the important role for the T4SS-dependent interaction of these receptors with H. pylori in the gastric epithelium.

• AGS
• BHY
• CAL-27
• CEACAM
• CagA
• HN
• Signaling
• T4SS
• Type IV secretion
• Tyrosine kinases

Helicobacter pylori is one of the major stomach microbiome components, promoting development of inflammation and gastric cancer in humans. H. pylori has a unique ability to transform into a coccoidal form which is difficult to detect by many diagnostic methods, such as urease activity detection, and even histopathological examination. Here we present a comparison of three methods for H. pylori identification: histological assessment (with eosin, hematoxylin, and Giemsa staining), polymerase chain reaction (PCR) detection of urease (ureA specific primers), and detection by 16S rRNA gene sequencing. The study employed biopsies from the antral part of the stomach (N = 40). All samples were assessed histologically which revealed H. pylori in eight patients. Bacterial DNA isolated from the bioptates was used as a template for PCR reaction and 16S rRNA gene sequencing that revealed H. pylori in 13 and in 20 patients, respectively. Thus, 16S rRNA gene sequencing was the most sensitive method for detection of H. pylori in stomach biopsy samples.

• Biopsy
• Helicobacter
• NGS
• Next-generation sequencing
• Pylori
• Sequencing
• Specimens
• Stomach

Investigating distinct individual- and household-level risk factors for acquiring Helicobacter pylori (H. pylori) infection can inform disease prevention efforts and implicate possible routes of transmission. This study determined the magnitude of H. pylori infection among schoolchildren in Ziway, central Ethiopia and identified personal and household correlates of H. pylori infection in young Ethiopian children.

A total of 434 schoolchildren participated in this cross-sectional study. Infection status was assessed using antigen and antibody rapid tests. Demographic and lifestyle information was obtained from parents via an interviewer-led questionnaire. Univariate and multivariate logistic regressions were performed to assess the relationships between potential individual- and household-level risk factors and H. pylori infection.

The prevalence of H. pylori infection was 65.7% (285/434). Of the personal variables assessed, the age group 10–14 years was found to be significantly associated with higher odds of H. pylori infection in univariate analysis (COR = 2.22, 95% CI: 1.06–4.66, p = 0.03) and remained positively correlated after adjusting for confounding factors. Of the household-level factors explored, having a traditional pit or no toilet was found to be significantly associated with 3.93-fold higher odds of H. pylori infection (AOR = 3.93, 95% CI: 1.51–10.3, p = 0.01), while the presence of smokers in the household was associated with 68% lower odds of infection (AOR = 0.32, 95% CI: 0.11–0.89, p = 0.03).

This study from a developing country provides additional evidence for older age as a personal risk factor for H. pylori infection and identifies correlations between socioeconomic and sanitation household factors and positive childhood infection status. The associations reported here support the hypothesized fecal-oralroute of transmission for H. pylori.

• Children
• Ethiopia
• H. pylori
• Risk factors

Helicobacter pylori infection is a significant burden to the public health in China as it can lead to various gastric diseases including peptic ulcers and gastric cancer. Since most infections occurred during childhood, it is therefore necessary to understand the prevalence and risk determinants of this bacterial infection in children. Herewith, we conducted a cross-sectional study in the Kuichong Subdistrict of Shenzhen City to assess the prevalence and risk factors of H. pylori infection among children.

From September 2018 to October 2018, 1,355 children aged 6–12 years from four primary schools in the Kuichong Subdistrict of Shenzhen City were recruited. These children were screened for H. pylori infection using the ¹³C-urea breath test. In addition, parents were requested to fill out a standardized questionnaire. The chi-square test and multivariable logistic regression analysis were used to identify risk factors for H. pylori.

Among 1,355 children recruited in this study, 226 (16.7%; 95% CI [14.7–18.7]) were positive of H. pylori infection. Multivariable logistic regression analysis identified six factors significantly associated with H. pylori infection children including parent(s) with tertiary education level (OR: 0.64; 95% CI [0.46–0.89]), testing bottle feed temperature using the mouth (OR: 1.79; 95% CI [1.19–2.68]), sharing of cutlery between the feeding person and young children during meals (OR: 1.84; 95% CI [1.22–2.78]), eating fruit after peeling (OR: 2.56; 95% CI [1.4–4.71]), frequent dining out (OR: 3.13; 95% CI [1.46–6.68]) and snacking (OR: 1.43; 95% CI [1.01–2.01]).

Overall, better educated parent(s) played a protective role against the acquisition of H. pylori infection in children. Testing bottle feed temperature using the mouth, cutlery sharing between the feeding person and young children, and snacking posed a lower but significant risk for H. pylori infection. Only eating peeled fruits and frequent dining out were associated with greater infection risks.

• Children
• China
• Helicobacter pylori
• Prevalence
• Risk factor
• Urea breath test

Helicobacter pylori (H. pylori) infects approximately 50% of the world population. The multiple gastrointestinal and extra-gastrointestinal diseases caused by H. pylori infection pose a major healthcare threat to families and societies; it is also a heavy economic and healthcare burden for countries that having high infection rates. Eradication of H. pylori is recommended for all infected individuals. Traditionally, “test and treat” and "screen and treat" strategies are available for various infected populations. However, clinical practice has noticed that these strategies have some shortfalls and may need refinement, mostly due to the fact that they are not easily manageable, and are affected by patient compliance, selection of treatment population and cost-benefit estimations. Furthermore, it is difficult to control infections from the source, therefore, development of additional, compensative strategies are encouraged to solve the above problems and facilitate bacteria eradication. H. pylori infection is a family-based disease, but few studies have been performed in a whole family-based approach to curb its intra-familial transmission and the development of related diseases. In this work, a third, novel whole family-based H. pylori eradication strategy is introduced. This approach screens, identifies, treats and follows up on all H. pylori-infected individuals in entire families to control H. pylori infection among family members, and reduce its long-term complications. This strategy is high-risk population-oriented, and able to reduce H. pylori spread among family members. It also has good patient-family compliance and, importantly, is practical for both high and low H. pylori-infected communities. Future efforts in these areas will be critical to initiate and establish healthcare policies and management strategies to reduce H. pylori-induced disease burden for society.

• Helicobacter pylori
• Intra-familial infection
• Gastrointestinal disease
• Gastric cancer

• Disease Eradication/methods
• Disease Transmission, Infectious/prevention & control
• Family
• Gastrointestinal Diseases/microbiology
• Gastrointestinal Diseases/prevention & control
• Helicobacter Infections/microbiology
• Helicobacter Infections/prevention & control
• Helicobacter Infections/transmission
• Helicobacter pylori
• Humans
• Stomach Neoplasms/microbiology
• Stomach Neoplasms/prevention & control

The correlation between Helicobacter pylori (H. pylori) and gastroesophageal reflux disease (GERD) is complex. Some studies showed a protective role of H. pylori infection against GERD. This study was aimed at assessing the role of H. pylori infection in GERD utilizing a large cohort of patients diagnosed with GERD.

All patients who underwent gastroscopy for an indication of GERD during the study period between 2015 and 2017 at the EMMS Nazareth Hospital were considered eligible for the study and therefore were included. H. pylori infection was determined by the rapid urease test or histology. Severity of esophagitis was assessed using the Los Angeles classification. Univariate analysis was performed to figure out differences between patients according to H. pylori infection status. Multivariate regression analysis was conducted to illustrate the predictors of positivity for H. pylori infection.

2,508 GERD patients were included with a median age of 49.42 ± 17.96 years. H. pylori infection was detected in 299 (11.9%) patients. GERD patients with H. pylori infection were found to be younger (48.83 ± 17.42 years versus 44.57 ± 17.69 years, p < 0.001), have the tendency to smoke more (1406 (63.6%) versus 266 (89.0%), p < 0.001), and use more proton pump inhibitors or PPIs (1314 (59.5%) versus 242 (80.9%), p < 0.001). In multivariate regression analysis, age (OR 0.987, p < 0.001), smoking status (OR 0.190, p < 0.001), use of ASA/NSAIDs (OR 1.652, p = 0.004), and use of statins (OR 0.499 (95%CI 0.295-0.846), p = 0.010) were found significant among H. pylori-positive individuals. H. pylori-positive subjects have less severe esophagitis and more hiatus hernia.

Patients with GERD and H. pylori infection were significantly younger, tended to smoke more, and used more PPIs and had significantly lower grades of esophagitis compared to noninfected ones.

Helicobacter pylori is one of the most common human pathogens that can cause gastrointestinal (GI) disorders, including simple gastritis, gastric ulcer, and malignant gastritis. In some cases, such as immunodeficiency and underlying diseases, it can be problematic as opportunistic infections. Diabetes mellitus (type 2) (T2DM) is one of the H. pylori underlying diseases. Since GI problems are observed in diabetic patients, it is necessary to treat H. pylori infection. In this review, we aimed to evaluate the possible relationship between H. pylori and T2DM according to epidemiological surveys of 70 studies retrieved from databases, including Scopus, PubMed, and Google Scholar about the relationship between H. pylori and T2DM, and discuss the reported background mechanisms of this correlation. According to the results of our study, the different studies have shown that H. pylori is more prevalent in Type 2 diabetic patients than healthy individuals or nondiabetic patients. The reason is development of H. pylori infection-induced inflammation and production of inflammatory cytokines as well as different hormonal imbalance by this bacterium, which are associated with diabetes mellitus. On the other hand, by tracing anti-H. pylori antibodies in patients with diabetes mellitus and occurrence of symptoms such as digestive problems in >75% of these patients, it can be concluded that there is a relationship between this bacterium and T2DM. Considering the evidence, it is crucially important that the probability of infection with H. pylori is evaluated in patients with T2DM so that medical process of the patient is followed with higher cautious.

• Diabetes
• Helicobacter pylori
• Type 2 diabetes
• diabetes mellitus

• Helicobacter pylori
• RAPD fingerprinting
• TnPZ
• intra-familial transmission

• Animals
• Bacterial Adhesion
• Child
• Disease Models, Animal
• Epithelial Cells/microbiology
• Family
• Female
• Gastric Mucosa/microbiology
• Genome, Bacterial
• Gerbillinae/microbiology
• Helicobacter Infections/microbiology
• Helicobacter pylori/isolation & purification
• Helicobacter pylori/pathogenicity
• Humans
• Infectious Disease Transmission, Vertical
• Male
• Stomach/microbiology
• Whole Genome Sequencing

• Antibiotic therapy
• Epidemiology
• Gastric cancer
• Helicobacter pylori
• Public health

• Helicobacter pylori
• anaerobic conditions
• culturability
• morphology

Gastric adenocarcinoma is globally the third leading cause of death due to malignancy, with the bulk of this disease burden being suffered by low and middle income countries (LMIC), especially in Asia. The majority of these cancers develop as a result of a chronic gastritis that arises in response to infection with the stomach-dwelling bacterium, Helicobacter pylori. A vaccine against this pathogen would therefore be a powerful tool for preventing gastric adenocarcinoma. However, notwithstanding a proof-of-concept that vaccination can protect children from acquisition of H. pylori infection, there are currently no advanced vaccine candidates with only a single vaccine in Phase I clinical trial. Further, the development of a vaccine against H. pylori is not a current strategic priority of major pharmaceutical companies despite the large global disease burden. Given the involvement of such companies is likely to be critical for late stage development, there is therefore a need for an increased appreciation of the burden of this disease in LMIC and more investment to reinvigorate research in H. pylori vaccine Research and Development.

• Helicobacter pylori
• Research and development
• Vaccine

• Gastric diseases
• Helicobacter pylori
• Mongolia
• Risk factors

• R01 DK062813 NIDDK NIH HHS
• Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan
• National Institute of Diabetes and Digestive and Kidney Diseases

• Animals
• Anti-Bacterial Agents/pharmacology
• Anti-Bacterial Agents/therapeutic use
• Breath Tests
• Helicobacter Infections/diagnosis
• Helicobacter Infections/drug therapy
• Helicobacter Infections/microbiology
• Helicobacter Infections/transmission
• Helicobacter pylori/drug effects
• Helicobacter pylori/physiology
• Humans
• Mouth/microbiology
• Oral Hygiene
• Periodontal Diseases/diagnosis
• Periodontal Diseases/drug therapy
• Periodontal Diseases/microbiology
• Periodontium/microbiology
• Stomach/microbiology
• Urea/metabolism

• Biprobe assay
• Fecal specimens
• Genotyping
• Helicobacter pylori
• qPCR

Epidemiologic studies have reported an inverse relationship between childhood Helicobacter pylori infection and development of allergic asthma. Because lung epithelium plays an important role in allergic asthma pathogenesis, we hypothesized that H. pylori may directly influence airway epithelial cell innate immune function, particularly in early childhood. To test our hypothesis, we established an in vitro H. pylori infection model using primary tracheobronchial epithelial cell cultures derived from infant, juvenile and adult rhesus monkeys. Airway epithelial cell cultures were infected with wild-type or cag pathogenicity island mutant H. pylori strains, followed by evaluation of IL-8 and IL-6 protein synthesis. We found that H. pylori primarily increased IL-8 synthesis in a MOI and age-dependent fashion, with a greater than 4-fold induction in infant versus adult cultures. H. pylori-induced IL-8 synthesis in infant and juvenile cultures was significantly reduced by cag pathogenicity island mutants, indicating a requirement for the type IV secretion system. Although peptidoglycan recognition of nucleotide binding oligomerization domain-containing protein 1 (NOD1) and NF-kappaB have been implicated as key cytokine signaling molecules for H. pylori infection in gastric epithelium, NOD1 (ML130) or NF-kappaB (JSH-23) inhibitors minimally affected IL-8 synthesis in airway epithelial cell cultures following H. pylori infection. In contrast, inhibition of the p38 MAP kinase pathway (SB203580) resulted in almost complete suppression of H. pylori-induced IL-8 synthesis. Collectively, these results indicate that H. pylori can preferentially elicit IL-8 synthesis in a model of pediatric airway epithelium using the type IV secretion system via p38 MAP kinase.

• Animals
• Bacterial Proteins/metabolism
• Cell Line
• Helicobacter Infections/metabolism
• Helicobacter pylori/metabolism
• Helicobacter pylori/physiology
• Humans
• In Vitro Techniques
• Interleukin-6/metabolism
• Interleukin-8/metabolism
• Primates
• Respiratory Mucosa/enzymology
• Respiratory Mucosa/immunology
• Respiratory Mucosa/microbiology
• Signal Transduction/physiology
• Type IV Secretion Systems/metabolism
• p38 Mitogen-Activated Protein Kinases/metabolism

• P51 OD011107 NIH HHS
• R01 HL097087 NHLBI NIH HHS
• R56 AI091893 NIAID NIH HHS
• T32 HL007013 NHLBI NIH HHS
• NIH Office of the Director
• National Institute of Allergy and Infectious Diseases
• National Heart, Lung, and Blood Institute

• Choroidal thickness
• Enhanced depth imaging optical coherence tomography (EDI-OCT)
• Helicobacter pylori eradication
• Helicobacter pylori infection
• Retinal nerve fiber layer thickness

幽门螺杆菌(Helicobacter pylori, H. pylori)与胃癌(gastric cancer, GC)发生发展密切相关, 根除H. pylori可降低GC发生率. 经济学分析表明, 在高危人群中根除治疗H. pylori作为预防GC的策略是成本效益较好的. 即使在GC低风险人群中, H. pylori筛查和治疗也能使上消化道其他非恶性疾病获益. 然而, 广泛开展H. pylori根除治疗可能带来其他问题, 包括抗生素耐药增加和与H. pylori负相关疾病(如胃食管反流病、Barrett食管、哮喘和肥胖等)的患病率升高. 本文将结合近年最新研究, 就上述问题展开论述, 进一步提出H. pylori根除治疗预防GC所面临的挑战以及将来可能的进展方向.

• 幽门螺杆菌
• 胃癌
• 根除治疗
• 人群筛查

• Children and Ghana
• H.pylori infection
• Immune chromatographic assay
• Prevalence

Among the human health conditions linked to microbial communities, phenotypes are often associated with only a subset of strains within causal microbial groups. Although it has been critical for decades in microbial physiology to characterize individual strains, this has been challenging when using culture-independent high-throughput metagenomics. We introduce StrainPhlAn, a novel metagenomic strain identification approach, and apply it to characterize the genetic structure of thousands of strains from more than 125 species in more than 1500 gut metagenomes drawn from populations spanning North and South American, European, Asian, and African countries. The method relies on per-sample dominant sequence variant reconstruction within species-specific marker genes. It identified primarily subject-specific strain variants (<5% inter-subject strain sharing), and we determined that a single strain typically dominated each species and was retained over time (for >70% of species). Microbial population structure was correlated in several distinct ways with the geographic structure of the host population. In some cases, discrete subspecies (e.g., for Eubacterium rectale and Prevotella copri) or continuous microbial genetic variations (e.g., for Faecalibacterium prausnitzii) were associated with geographically distinct human populations, whereas few strains occurred in multiple unrelated cohorts. We further estimated the genetic variability of gut microbes, with Bacteroides species appearing remarkably consistent (0.45% median number of nucleotide variants between strains), whereas P. copri was among the most plastic gut colonizers. We thus characterize here the population genetics of previously inaccessible intestinal microbes, providing a comprehensive strain-level genetic overview of the gut microbial diversity.