• Crohn’s disease
• H. pylori
• immune modulation
• inflammatory bowel disease
• intestinal microbiota
• ulcerative colitis

• Britannilactone 1-O-acetate
• Gastroesophageal reflux disease
• NLRP3
• Reflux esophagitis
• TRIM31

• Grant No. XZR2021076 Natural Science Foundation project of Nanjing University of Chinese Medicine
• Grant No. SKY2022076) Suzhou science and technology plan project

• Helicobacter pylori
• antibiotics
• disease activity
• eradication
• inflammatory bowel disease

• CiteSpace
• VOSviewer
• bibliometric analysis
• helicobacter pylori
• inflammatory bowel disease

• Helicobacter pylori
• Mendelian randomization
• eosinophilic esophagitis
• inflammatory factors
• mediation analysis

• Humans
• Mendelian Randomization Analysis
• Helicobacter Infections/immunology
• Helicobacter Infections/complications
• Eosinophilic Esophagitis/immunology
• Eosinophilic Esophagitis/genetics
• Eosinophilic Esophagitis/epidemiology
• Eosinophilic Esophagitis/etiology
• Eosinophilic Esophagitis/microbiology
• Helicobacter pylori/immunology
• Antibodies, Bacterial/blood
• Antibodies, Bacterial/immunology
• Immunoglobulin G/blood
• Immunoglobulin G/immunology
• Polymorphism, Single Nucleotide
• Cytokines
• Genetic Predisposition to Disease

• Crohn’s disease
• H. pylori
• IBD
• diagnosis
• eradication
• immunological modulation
• inflammatory bowel disease
• molecular biology
• ulcerative colitis

• Helicobacter pylori
• antibiotics
• colorectal cancer
• eradication therapy
• immune response
• intestinal microbiome

• Humans
• Helicobacter Infections/complications
• Helicobacter Infections/microbiology
• Gastrointestinal Microbiome
• Helicobacter pylori/physiology
• Stomach/microbiology
• Anti-Bacterial Agents/therapeutic use
• Anti-Bacterial Agents/pharmacology
• Colorectal Neoplasms/epidemiology
• Colorectal Neoplasms/etiology

• Colitis
• Gut microbiota
• In vitro fermentation
• Inflammation
• Vitexin

• Humans
• Mice
• Animals
• Gastrointestinal Microbiome
• Cytokines/metabolism
• Colitis/chemically induced
• Colitis/drug therapy
• Colitis/metabolism
• Inflammation
• Bacteria/metabolism
• Dextran Sulfate/adverse effects
• Disease Models, Animal
• Mice, Inbred C57BL
• Colon/metabolism

• 2022YFF1100104 National Key R&D Program of China
• No. 31901609 National Natural Science Foundation of China

• Cytotoxin-associated antigen A oncoprotein
• Gut microbiota
• Helicobacter pylori
• Helicobacter pylori neutrophil-activating protein
• Immunological modulation
• Inflammatory bowel disease
• NLR family pyrin domain containing 3 inflammasome

• Humans
• Helicobacter pylori
• Helicobacter Infections/complications
• Immunity, Innate
• Inflammatory Bowel Diseases
• Stomach

• Allopurinol
• Fecal microbiota transplantation
• Gout arthritis
• Gut microbiota
• Simiao decoction

• LY21H270006 Science Fund for Distinguished Young Scholars of Zhejiang Province

• BRCC3
• CD82
• Colitis
• Inflammation
• NLRP3

• Animals
• Mice
• Colitis/metabolism
• Dextran Sulfate
• Inflammasomes/metabolism
• Mice, Inbred C57BL
• NLR Family, Pyrin Domain-Containing 3 Protein/metabolism

• National Research Foundation of Korea (NRF)
• Hanyang University (HYU)

• Autophagy
• Helicobacter pylori
• NLRP3 inflammasome
• ROS
• TRIM31

• Helicobacter pylori
• Hp0169
• Hp1012
• HtrA
• Proteases

• Humans
• Peptide Hydrolases
• Helicobacter pylori/genetics
• Helicobacter Infections/drug therapy
• Endopeptidases
• Stomach Diseases

• I 4360 Austrian Science Fund FWF
• P 31507 Austrian Science Fund FWF

• H. pylori
• Immune evasion
• Immune response
• Persistence

• Humans
• Helicobacter pylori
• Persistent Infection
• Stomach Neoplasms
• Biology

• H. pylori eradication
• bacterial interaction
• gastric diseases
• gastric microecology
• microbiota transplant

• Apoptosis
• Autophagy
• Ethanol
• HMGB1
• Irbesartan
• NLRP3 inflammasome

• AMP-Activated Protein Kinases/metabolism
• Angiotensin Receptor Antagonists/pharmacology
• Animals
• Anti-Inflammatory Agents/pharmacology
• Antioxidants/pharmacology
• Apoptosis
• Autophagy
• Beclin-1/metabolism
• Caspase 3/metabolism
• Cytokines/metabolism
• Ethanol/adverse effects
• Gastric Mucosa/metabolism
• HMGB1 Protein/metabolism
• Inflammasomes/metabolism
• Inflammation/metabolism
• Irbesartan/pharmacology
• NF-E2-Related Factor 2/metabolism
• NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
• Omeprazole/pharmacology
• Peroxisome Proliferator-Activated Receptors
• Rats
• Rats, Wistar
• Reactive Oxygen Species/metabolism
• Stomach Ulcer/chemically induced
• TOR Serine-Threonine Kinases/metabolism
• bcl-2-Associated X Protein/metabolism

Recently, studies have suggested a role for the gut microbiota in epilepsy. Gut microbial changes during ketogenic diet (KD) treatment of drug-resistant epilepsy have been described. Inflammation is associated with certain types of epilepsy and specific inflammation markers decrease during KD. The gut microbiota plays an important role in the regulation of the immune system and inflammation.

28 children with drug-resistant epilepsy treated with the ketogenic diet were followed in this observational study. Fecal and serum samples were collected at baseline and three months after dietary intervention.

We identified both gut microbial and inflammatory changes during treatment. KD had a general anti-inflammatory effect. Novel bioinformatics and machine learning approaches identified signatures of specific Bifidobacteria and TNF (tumor necrosis factor) associated with responders before starting KD. During KD, taxonomic and inflammatory profiles between responders and non-responders were more similar than at baseline.

Our results suggest that children with drug-resistant epilepsy are more likely to benefit from KD treatment when specific Bifidobacteria and TNF are elevated. We here present a novel signature of interaction of the gut microbiota and the immune system associated with anti-epileptic response to KD treatment. This signature could be used as a prognostic biomarker to identify potential responders to KD before starting treatment. Our findings may also contribute to the development of new anti-seizure therapies by targeting specific components of the gut microbiota.

This study was supported by the Swedish Brain Foundation, Margarethahemmet Society, Stiftelsen Sunnerdahls Handikappfond, Linnea & Josef Carlssons Foundation, and The McCormick Genomic & Proteomic Center.

• Bifidobacterium
• Bioinformatics
• Epilepsy
• Gut microbiota
• Inflammation
• Ketogenic diet
• Machine learning
• Omics
• TNF

• Gastric Mucosa
• Helicobacter Infections/complications
• Helicobacter pylori
• Humans
• Immunotherapy/adverse effects
• Lymphoma, B-Cell, Marginal Zone/pathology

• Swiss Cancer Research Foundation

• autoimmunity
• fibrosis
• infection
• inflammation
• post-translational modification
• sialic acid
• sialidase

• Animals
• Glycoproteins/metabolism
• Immune System Diseases
• Mammals/metabolism
• Mucins
• N-Acetylneuraminic Acid/metabolism
• Neuraminidase/metabolism

• R21 AI144497 NIAID NIH HHS
• National Institute of Allergy and Infectious Diseases
• U.S. Department of Defense

The modern Gastroenterology have witnessed an essential stride since Helicobacter pylori was first found in the stomach and then its pathogenic effect was discovered. According to the researches conducted during the nearly 40 years, it has been found that this bacterium is associated with a natural history of many upper gastrointestinal diseases. Epidemiological data show an increased incidence of autoimmune disorders with or after infection with specific microorganisms. The researches have revealed that H. pylori is a potential trigger of gastric autoimmunity, and it may be associated with other autoimmune diseases, both innate and acquired. This paper reviews the current support or opposition about H. pylori as the role of potential triggers of autoimmune diseases, including inflammatory bowel disease, autoimmune thyroiditis, type 1 diabetes mellitus, autoimmune liver diseases, rheumatoid arthritis, idiopathic thrombocytopenic purpura, systemic lupus erythematosus, as well as Sjogren’s syndrome, chronic urticaria and psoriasis, and tried to explain the possible mechanisms.

• Helicobacter pylori
• autoimmune diseases
• pathogenesis
• relationship
• review

• celiac disease
• inflammatory bowel disease
• irritable bowel syndrome
• management
• microscopic colitis

• Ministry of Science and Technology of the People''s Republic of China
• Natural Science Foundation of Henan Province
• Henan University of Technology

• Helicobacter pylori
• cancer
• cancer immunobiology
• immunotherapy

Helicobacter pylori (H. pylori) is generally regarded as a human pathogen and a class 1 carcinogen, etiologically related to gastric and duodenal ulcers, gastric cancer, and mucosa-associated lymphoid tissue lymphoma. However, H. pylori can also be regarded as a commensal symbiont. Unlike other pathogenic/ opportunistic bacteria, H. pylori colonization in infancy is facilitated by T helper type 2 immunity and leads to the development of immune tolerance. Fucosylated gastric mucin glycans, which are an important part of the innate and adaptive immune system, mediate the adhesion of H. pylori to the surface of the gastric epithelium, contributing to successful colonization. H. pylori may have beneficial effects on the host by regulating gastrointestinal (GI) microbiota and protecting against some allergic and autoimmune disorders and inflammatory bowel disease. The potential protective role against inflammatory bowel disease may be related to both modulation of the gut microbiota and the immunomodulatory properties of H. pylori. The inverse association between H. pylori and some potentially proinflammatory and/or procarcinogenic bacteria may suggest it regulates the GI microbiota. Eradication of H. pylori can cause various adverse effects and alter the GI microbiota, leading to short-term or long-term dysbiosis. Overall, studies have shown that gastric Actinobacteria decrease after H. pylori eradication, Proteobacteria increase during short-term follow-up and then return to baseline levels, and Enterobacteriaceae and Enterococcus increase in the short-term and interim follow-up. Various gastric mucosal bacteria (Actinomyces, Granulicatella, Parvimonas, Peptostreptococcus, Prevotella, Rothia, Streptococcus, Rhodococcus, and Lactobacillus) may contribute to precancerous gastric lesions and cancer itself after H. pylori eradication. H. pylori eradication can also lead to dysbiosis of the gut microbiota, with increased Proteobacteria and decreased Bacteroidetes and Actinobacteria. The increase in gut Proteobacteria may contribute to adverse effects during and after eradication. The decrease in Actinobacteria, which are pivotal in the maintenance of gut homeostasis, can persist for > 6 mo after H. pylori eradication. Furthermore, H. pylori eradication can alter the metabolism of gastric and intestinal bacteria. Given the available data, eradication cannot be an unconditional recommendation in every case of H. pylori infection, and the decision to eradicate H. pylori should be based on an assessment of the benefit–risk ratio for the individual patient. Thus, the current guidelines based on the unconditional “test-and-treat” strategy should be revised. The most cautious and careful approach should be taken in elderly patients with multiple eradication failures since repeated eradication can cause antibiotic-associated diarrhea, including severe Clostridioides difficile-associated diarrhea and colitis and antibiotic-associated hemorrhagic colitis due to Klebsiella oxytoca. Furthermore, since eradication therapy with antibiotics and proton pump inhibitors can lead to serious adverse effects and/or dysbiosis of the GI microbiota, supplementation of probiotics, prebiotics, and microbial metabolites (e.g., butyrate + inulin) should be considered to decrease the negative effects of eradication.

• Helicobacter pylori
• Eradication
• Gastrointestinal microbiota
• Dysbiosis
• Fucosylated glycan
• Inflammatory bowel disease

• Aged
• Dysbiosis/microbiology
• Gastric Mucosa/pathology
• Gastrointestinal Microbiome
• Helicobacter Infections/microbiology
• Helicobacter pylori
• Humans

• Apoptosis
• Autophagy
• Ethanol
• Inflammasome
• Oxidative stress
• Saxagliptin

• AMP-Activated Protein Kinase Kinases
• Adamantane/analogs & derivatives
• Adamantane/therapeutic use
• Animals
• Autophagy/drug effects
• Dipeptides/therapeutic use
• Dipeptidyl-Peptidase IV Inhibitors/therapeutic use
• Ethanol/adverse effects
• Inflammasomes/antagonists & inhibitors
• Inflammasomes/metabolism
• Male
• NLR Family, Pyrin Domain-Containing 3 Protein/antagonists & inhibitors
• NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
• Protein Kinases/metabolism
• Rats, Wistar
• Signal Transduction/drug effects
• Stomach Diseases/chemically induced
• Stomach Diseases/drug therapy
• Stomach Diseases/pathology
• TOR Serine-Threonine Kinases/metabolism
• Rats

Jinmaitong (JMT), a compound prescription of traditional Chinese medicine, has long been used as a therapy for diabetic peripheral neuropathy (DPN). However, the neuroprotective mechanisms of JMT and its effect on gut microbiota remained unknown. Here, we examined the effects of JMT on behavior, pathomorphology and gut microbiota in streptozotocin (STZ)-induced DPN rats. Compared to distilled water administration, JMT reversed decreases in mechanical withdraw threshold and intraepidermal nerve fiber density, improved neurological morphology of sciatic nerves, increased serum neuregulin 1 (NRG1) level and contactin-associated protein (Caspr)-positive paranodes, and decreased amyloid precursor protein (APP) accumulation in DPN rats. More importantly, JMT enriched nine species of the gut microbiota of DPN rats, helping to prevent dysbiosis. Among these species, p_Actinobacteria, p_Proteobacteria and c_Actinobacteria were negatively correlated with DPN phenotypes and positively correlated with serum NRG1 level. These results indicate that JMT may exert a neuroprotective effect by modulating phenotype-associated gut microbiota and increasing serum NRG1 level in STZ-induced DPN rats. JMT may therefore be an effective complementary and alternative anti-DPN therapy.

• diabetic complications
• diabetic peripheral neuropathy
• gut microbiota
• jinmaitong
• neuregulin 1

• LGM2605
• antioxidant
• inflammation
• ketogenesis
• lipid steatosis
• oxidative stress
• retina
• small molecule therapeutics

• Antioxidants/metabolism
• Autophagy
• Butylene Glycols/pharmacology
• Cell Line
• Cytokines
• Gene Expression
• Glucosides/pharmacology
• Humans
• Inflammation/metabolism
• Lignans/chemistry
• Lignans/metabolism
• Lipid Metabolism
• Lipids
• Mitochondria/metabolism
• Oxidation-Reduction
• Oxidative Stress/drug effects
• Phagocytosis
• Phagosomes/metabolism
• Retinal Pigment Epithelium/metabolism
• Retinal Pigments/genetics
• Retinal Pigments/metabolism

• R01 EY026525 NEI NIH HHS
• 001 Schoenleber Award University of Pennsylvania
• P30 EY001583 NEI NIH HHS
• P30 EY 001583 NEI NIH HHS
• EY026525 NEI NIH HHS

• Antibacterial
• Cytidine/uridine monophosphate kinase 2
• Intestinal barrier
• Triploid crucian carp

• Aeromonas hydrophila/physiology
• Amino Acid Sequence
• Animals
• Bacterial Infections/immunology
• Bacterial Infections/veterinary
• Carps/genetics
• Carps/immunology
• DNA, Mitochondrial/biosynthesis
• Disease Resistance/genetics
• Disease Resistance/immunology
• Fish Diseases/immunology
• Fish Proteins/genetics
• Fish Proteins/immunology
• Fish Proteins/metabolism
• Gene Expression
• Inflammasomes/metabolism
• Intestinal Mucosa/immunology
• Intestinal Mucosa/microbiology
• NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
• Nucleoside-Phosphate Kinase/genetics
• Nucleoside-Phosphate Kinase/immunology
• Nucleoside-Phosphate Kinase/metabolism
• Triploidy

• IBD
• Parkinson disease
• cardiovascular diseases
• cirrhosis
• diabetes
• metabolic syndrome

• NLRP3 inflammasome
• gut
• lung
• microbiome
• microbiota

• Asthma
• Helicobacter pylori
• allergy
• microbiome

• enteric infection
• epidemiology
• pathogenesis
• microbiome
• mucosal immunology

• Colitis, Ulcerative/epidemiology
• Communicable Diseases/complications
• Communicable Diseases/epidemiology
• Crohn Disease/complications
• Crohn Disease/epidemiology
• Gastrointestinal Diseases/complications
• Gastrointestinal Diseases/epidemiology
• Helicobacter pylori/immunology
• Humans
• Incidence
• Inflammatory Bowel Diseases/epidemiology
• Inflammatory Bowel Diseases/etiology
• Prospective Studies
• Risk Factors

• IK2 CX002027 CSRD VA
• K12 HS026395 AHRQ HHS
• P30 DK058404 NIDDK NIH HHS

• Emigrants and immigrants
• access
• and evaluation
• epidemiology
• healthcare quality
• immune system diseases
• public health

• Allergy
• Bacteria
• Digestive System
• Immune System Diseases

• bacteria
• digestive system
• immune system diseases
• epidemiology
• allergy

The gastric lamina propria of mice that have been experimentally infected with the pathobiont Helicobacter pylori hosts a dense network of myeloid cells that includes BATF3-dependent CD103⁺ dendritic cells (DCs). We show here that CD103⁺ DCs are strictly required for gastric Th1 responses to H. pylori and for H. pylori infection control. A similar dependence of type 1 immunity on CD103⁺ DCs is observed in a Mycobacterium bovis BCG infection model, and in a syngeneic colon cancer model. Strikingly, we find that not only the expansion and/or recruitment of Th1 cells, but also of peripherally induced, neuropilin-negative regulatory T-cells to sites of infection requires BATF3-dependent DCs. A shared feature of the examined models is the strongly reduced production of the chemokines and CXCR3 ligands CXCL9, 10 and 11 in BATF3-deficient mice. The results implicate BATF3-dependent DCs in the recruitment of CXCR3⁺ effector and regulatory T-cells to target tissues and in their local expansion.

In this work, Arnold & Zhang et al report that CD103⁺ DCs are required for protective Th1 responses, infection control of mucosal and systemic bacterial pathogens, and anti-tumor immunity driven by CD4⁺ Th1 cells and CD8⁺ T cells. CD103⁺ DCs further specifically promote the recruitment of Tbet⁺ peripherally induced Tregs to sites of infection. The results implicate CD103⁺ DCs in the trafficking of CXCR3⁺ Tbet⁺ T-cells to sites of infection and tumorigenesis.

Autoimmune atrophic gastritis (AAG) is associated with an increased risk of certain types of gastric cancer (GC). Helicobacter pylori (H. pylori) infection may have a role in the induction and/or maintenance of AAG and GC. Toll-like receptors (TLR) are essential for H. pylori recognition and subsequent innate and adaptive immunity responses. This study therefore aimed to characterize TLR polymorphisms, and features of bacterial flagellin A in samples from patients with AAG (n = 67), GC (n = 114) and healthy donors (HD; n = 97). TLR5 rs5744174 C/C genotype was associated with GC, lower IgG anti H. pylori response and a higher H. pylori flagellin A abundance and motility. In a subset of patients with AAG, H. pylori strains showed a reduction of the flagellin A abundance and a moderate motility compared with strains from GC patients, a prerequisite for active colonization of the deeper layers of the mucosa, host immune response and inflammation. TLR9 rs5743836 T allele showed an association with serum gastrin G17. In conclusion, our study suggests that alterations of flaA protein, moderate motility in H. pylori and two polymorphisms in TLR5 and TLR9 may favor the onset of AAG and GC, at least in a subset of patients. These findings corroborate the function of pathogen–host cell interactions and responses, likely influencing the pathogenetic process.

• Helicobacter pylori
• autoimmune gastritis
• flagellin A
• toll-like receptor 5 (TLR5)
• toll-like receptor 9 (TLR9)

Helicobacter pylori has coexisted with humans for at least 60.000 years and has evolved persistence strategies that allow it to evade host immunity and colonize its host for life. The VacA protein is expressed by all H. pylori strains and is required for high-level persistent infection in experimental mouse models. Here, we show that VacA targets myeloid cells in the gastric mucosa to create a tolerogenic environment that facilitates regulatory T-cell differentiation, while suppressing effector T-cell priming and functionality. Tregs that are induced in the periphery during H. pylori infection can be found not only in the stomach but also in the lungs of infected mice, where they are likely to affect immune responses to allergens.

The gastric bacterium Helicobacter pylori causes a persistent infection that is directly responsible for gastric ulcers and gastric cancer in some patients and protective against allergic and other immunological disorders in others. The two outcomes of the Helicobacter-host interaction can be modeled in mice that are infected as immunocompetent adults and as neonates, respectively. Here, we have investigated the contribution of the Helicobacter immunomodulator VacA to H. pylori-specific local and systemic immune responses in both models. We found that neonatally infected mice are colonized at higher levels than mice infected as adults and fail to generate effector T-cell responses to the bacteria; rather, T-cell responses in neonatally infected mice are skewed toward Foxp3-positive (Foxp3⁺) regulatory T cells that are neuropilin negative and express RORγt. We found these peripherally induced regulatory T cells (pTregs) to be enriched, in a VacA-dependent manner, not only in the gastric mucosa but also in the lungs of infected mice. Pulmonary pTreg accumulation was observed in mice that have been infected neonatally with wild-type H. pylori but not in mice that have been infected as adults or mice infected with a VacA null mutant. Finally, we traced VacA to gastric lamina propria myeloid cells and show that it suppressed interleukin-23 (IL-23) expression by dendritic cells and induced IL-10 and TGF-β expression in macrophages. Taken together, the results are consistent with the idea that H. pylori creates a tolerogenic environment through its immunomodulator VacA, which skews T-cell responses toward Tregs, favors H. pylori persistence, and affects immunity at distant sites.

• T cells
• T-cell immunity
• dendritic cells
• host-cell interactions
• immunomodulation
• macrophages
• mucosal infection
• regulatory T cells

• RFP(+)H. pylori
• dendritic cells
• humanized mice
• immune regulation
• inflammasome activation
• innate immune receptors
• sampling and antigen processing

• Crohn's disease
• NLRP3 inflammasome
• gut homeostasis
• mucosal immune
• ulcerative colitis

Colorectal cancer (CRC) is one of the most common malignancies worldwide. Inflammation contributes to cancer development and inflammatory bowel disease is an important risk factor for CRC. The aim of this study is to assess whether a widely used probiotic Enterococcus faecalis can modulate the NLRP3 inflammasome and protect against colitis and colitis-associated CRC. We studied the effect of heat-killed cells of E. faecalis on NLRP3 inflammasome activation in THP-1-derived macrophages. Pretreatment of E. faecalis or NLRP3 siRNA can inhibit NLRP3 inflammasome activation in macrophages in response to fecal content or commensal microbes, P. mirabilis or E. coli, according to the reduction of caspase-1 activation and IL-1β maturation. Mechanistically, E. faecalis attenuates the phagocytosis that is required for the full activation of the NLRP3 inflammasome. In in vivo mouse experiments, E. faecalis can ameliorate the severity of intestinal inflammation and thereby protect mice from dextran sodium sulfate (DSS)-induced colitis and the formation of CRC in wild type mice. On the other hand, E. faecalis cannot prevent DSS-induced colitis in NLRP3 knockout mice. Our findings indicate that application of the inactivated probiotic, E. faecalis, may be a useful and safe strategy for attenuation of NLRP3-mediated colitis and inflammation-associated colon carcinogenesis.

• NLRP3
• cancer
• colitis
• inflammasome
• probiotic

• Adenosine Triphosphate/pharmacology
• Animals
• Colitis/chemically induced
• Colitis/complications
• Colorectal Neoplasms/etiology
• Colorectal Neoplasms/prevention & control
• Dextran Sulfate/toxicity
• Enterococcus faecalis
• Gene Expression Regulation/drug effects
• Hot Temperature
• Inflammasomes/drug effects
• Interleukin-1beta
• Mice
• NLR Family, Pyrin Domain-Containing 3 Protein/genetics
• NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
• Nigericin/pharmacology
• Phagocytosis
• Probiotics

• Autoimmune diseases
• Autoimmunity
• Cross reactions
• Cross-reactivity
• Molecular mimicry

• Caspases
• Helicobacter pylori
• IL-1β
• Inflammasome
• Virulence factors

• Animals
• Dendritic Cells/metabolism
• Gastric Mucosa/metabolism
• Gastric Mucosa/pathology
• Gastrointestinal Tract/metabolism
• Gastrointestinal Tract/pathology
• Helicobacter Infections/metabolism
• Helicobacter Infections/pathology
• Humans
• Inflammatory Bowel Diseases/metabolism
• Inflammatory Bowel Diseases/pathology

• National Natural Science Foundation of China (National Science Foundation of China) - 81570507
• National Natural Science Foundation of China (National Science Foundation of China) - 81702314 Funding Program for Excellent Talents of Beijing(2017000021469G212)

• Aryl hydrocarbon receptor
• Cardamonin
• Inflammatory bowel disease
• NLRP3 inflammasome