Helicobacter pylori (H. pylori) is considered the main cause of gastritis, peptic ulcer and gastric carcinoma in the human populations. H. pylori infection influences the secretion level of several proinflammatory cytokines including IL-1β, which encoded by the IL-1B gene.

The current study aimed to investigate whether IL-1B gene polymorphisms are associated with H. pylori infection among the Jordanian population and responses to triple therapy.

The gastroscopic examination was performed on 412 subjects for H. pylori infection diagnosis, 257 subjects were found to be infected by H. Pylori (positive cases), whereas 155 subjects were uninfected (negative controls). The IL-1B gene T-31C and C3954T polymorphisms were genotyped by PCR-RFLP.

It was found that the T-31C polymorphism has a significant association with H. pylori infection (P<0.05), and the TT genotype frequency was significantly higher in infected subjects (50.2%) compared to controls (38.7%). On the other hand, no significant association was detected between C3954T SNPs and H. pylori infection among the Jordanian population. In addition, none of the examined polymorphisms were found to influence the responses to triple therapy.

The IL-1B gene T-31C SNP might be associated with an enhanced risk of H. pylori infection among the Jordanian population.

• Helicobacter pylori
• IL-1β
• IL1B gene
• interleukins
• single nucleotide polymorphism

• Helicobacter pylori
• environmental factors
• human genetic factors
• peptic ulcer
• stomach cancer

Baicalin (BA) has been shown to have anti-inflammatory and antioxidant activity. Zinc is a nutrient element.

This study is aimed at investigating the antichronic gastric ulcer activity of Zn-Baicalin complex (BA-Zn) and its related mechanisms in an acetic acid-induced gastric ulcer rat model.

The severely ulcerated gastric mucosa of model rats had lower GSH-Px (52.21 ± 7.13) and SOD (7.03 ± 0.10) activity, and higher MDA (2.39 ± 0.03) content compared to sham rats. BA-Zn reduced the gastric ulcer index in a dose-dependent manner, significantly increased SOD activity and GSH-Px level, and reduced the MDA content and IL-8 and TNF-α levels in the gastric mucosa. BA-Zn (6.5 and 13 mg/kg) exerted a greater antiulcerogenic effect than both BA and zinc-gluconate, leading to a reduced ulcer index (18.43 ± 1.11, 15.00 ± 1.44), decreased MDA content (1.33 ± 0.07, 0.63 ± 0.01), and increased SOD activity (17.62 ± 0.11, 20.12 ± 0.32) and GSH-Px levels (102.12 ± 9.11, 120.25 ± 9.07). In addition, our results from Western blot suggested that BA-Zn (6.5 and 13 mg/kg) has a greater antiulcerogenic effect than both BA and zinc-gluconate.

The BA-Zn complex possesses greater antichronic gastric ulcer properties compared to BA and zinc-gluconate due to its ability of oxidation resistance and anti-inflammatory effects.

Associations between interleukin-8 (IL-8) gene polymorphisms and periodontitis susceptibility have been investigated in many published studies, but the conclusions are still inconsistent. Therefore, we performed this systematic review and meta-analysis to review which polymorphisms have been researched and to obtain a precise result of the same polymorphism from different studies.

Finally 10 publications involving 1938 patients and 1569 controls were yielded, including 12 polymorphisms. Six studies investigated rs4073 polymorphism; two focused on rs2227306 and rs2227307; two referred to rs2227532 and T-738A; one detected rs2230054, rs1126579 and rs1126580; one inspected A2767T, T₁1722T₂ and C1633T, and one for rs2234671 polymorphism. Of them, IL-8 C1633T and rs1126580 polymorphisms showed positive association while the other ten polymorphisms revealed negative results.

A comprehensive literature search from PubMed, Web of Science, and Chinese National Knowledge Infrastructure was conducted for all potentially relevant studies published before January 2, 2017. Two authors selected the studies and extracted data. The pooled analysis was conducted using the RevMan 5.1 software if a polymorphism was reported by two or more studies.

Based on current evidence, the IL-8 rs4073, A2767T, T₁1722T₂, rs2234671, rs2230054, rs1126579, rs2227306, rs2227307, rs2227532, and T-738A polymorphisms were not associated with periodontitis susceptibility; the IL-8 C1633T and rs1126580 polymorphisms were associated with increased risk of periodontitis.

• interleukin-8
• meta-analysis
• periodontal diseases
• periodontitis
• polymorphism

• CYP2C19
• Helicobacter pylori
• host genetic polymorphism
• peptic ulcer disease
• prostate stem cell antigen
• virulence factors

• Case-control study
• disease susceptibility
• interleukin-8
• meta-analysis
• periodontitis
• polymorphism, genetic

• Case-control study
• Gene polymorphism
• Interleukin-8
• Osteoarthritis

Helicobacter pylori (H. pylori) is still the most prevalent infection of the world. Colonization of the stomach by this agent will invariably induce chronic gastritis which is a low-grade inflammatory state leading to local complications (peptic ulcer, gastric cancer, lymphoma) and remote manifestations. While H. pylori does not enter circulation, these extragastric manifestations are probably mediated by the cytokines and acute phase proteins produced by the inflammed mucosa. The epidemiologic link between the H. pylori infection and metabolic changes is inconstant and controversial. Growth delay was described mainly in low-income regions with high prevalence of the infection, where probably other nutritional and social factors contribute to it. The timely eradication of the infection will lead to a more healthy development of the young population, along with preventing peptic ulcers and gastric cancer An increase of total, low density lipoprotein and high density liporotein cholesterol levels in some infected people creates an atherogenic lipid profile which could promote atherosclerosis with its complications, myocardial infarction, stroke and peripheral vascular disease. Well designed and adequately powered long-term studies are required to see whether eradication of the infection will prevent these conditions. In case of glucose metabolism, the most consistent association was found between H. pylori and insulin resistance: again, proof that eradication prevents this common metabolic disturbance is expected. The results of eradication with standard regimens in diabetics are significantly worse than in non-diabetic patients, thus, more active regimens must be found to obtain better results. Successful eradication itself led to an increase of body mass index and cholesterol levels in some populations, while in others no such changes were encountered. Uncertainities of the metabolic consequences of H. pylori infection must be clarified in the future.

• Diabetes mellitus
• Cytokines
• Glucose homeostasis
• Growth
• Helicobacter pylori
• Interleukins
• Lipid metabolism
• Metabolic syndrome

• Animals
• Anti-Bacterial Agents/therapeutic use
• Blood Glucose/metabolism
• Diabetes Mellitus, Type 2/blood
• Diabetes Mellitus, Type 2/epidemiology
• Diabetes Mellitus, Type 2/microbiology
• Dyslipidemias/blood
• Dyslipidemias/epidemiology
• Dyslipidemias/microbiology
• Helicobacter Infections/blood
• Helicobacter Infections/drug therapy
• Helicobacter Infections/epidemiology
• Helicobacter Infections/microbiology
• Helicobacter pylori/drug effects
• Helicobacter pylori/growth & development
• Host-Pathogen Interactions
• Humans
• Inflammation Mediators/blood
• Insulin Resistance
• Lipids/blood
• Metabolic Syndrome/blood
• Metabolic Syndrome/epidemiology
• Metabolic Syndrome/microbiology
• Risk Factors
• Treatment Outcome

• Duodenal Ulcer/genetics
• Humans
• Polymorphism, Single Nucleotide
• Tumor Necrosis Factor-alpha/genetics