The association between cagL and cagA, vacAs-m, babA genes in patients with gastric cancer, duodenal ulcer, and non-ulcer dyspepsia related to Helicobacter pylori.

INTRODUCTION: As a component of the cag T4SS, the cagL gene is involved in the translocation of CagA into host cells and is essential for the formation of cag PAI-associated pili between H. pylori and gastric epithelial cells. AIM: We aimed to investigate the clinical association of the cagL gene with other virulence factors (VacA, CagA, EPIYA-C, and BabA protein) of H. pylori strains isolated from GC, duodenal ulcer (DU), and non-ulcer dyspepsia (NUD) cases. METHODS: The patient group (PG), including 47 patients (22 GC and 25 DU) and a 25 control group (CG= NUD) were included. Amplification of the H. pylori cagL, cagA, vacA, and babA2 genes and typing of EPIYA motifs were performed by PCR methods. RESULTS: Sixty-one (84.7%) H. pylori strains were detected with cagL (93.6% in SG, 68% in CG). We detected a significant difference between SG and CG for the presence of cagL (p=0.012) but no statistical comparison was done for (≥2) EPIYA-C repeats In the comparison of H. pylori strains with cagA/vacAs1m1 and cagA/ vacAs1m2 and babA2 for the presence of cagL, we could not detect a significant difference (p=1). CONCLUSION: We detected a significant difference between groups for the presence of cagL genotype (p=0.012). The vacAs1m1 (OR: 2.829), genotypes increased the GC and DU risk by 2.8 times, while multiple (≥2) EPIYA-C repeats incresed the GC and DU risk by 3.524 times. Gender (to be female) (OR: 0.454) decreased the GC and DU risk by inversly decreased in the multivariate analysis.

Should we leave the paper currency? A microbiological examination.

OBJECTIVE: Pathogens can be transmitted to banknotes due to the personal unhygienic habits. The aim of study was to find the possible pathogens on the banknotes circulating in the market and also to present their antibacterial resistance and their various virulence factors using genotypic and phenotypic methods. METHODS: A total of 150 samples of bank-notes were randomly collected between August 2017 and March 2018. VITEK systems were used for identification and antimicrobial susceptibility testing respectively. Antimicrobial resistance genes (mecA, van, extended-spectrum ß-lactamase [ESBL] and carbapenemases) and staphyloccoccal virulence genes (staphyloccoccal enterotoxins [SEs], pvl, and tsst-1) were determined using with real-time PCR. RESULTS: Staphylococcus aureus, coagulase-negative staphylococci (CoNS), Enterococcus spp., Gram-negative enteric bacteria, non-fermentative Gram-negative bacteria and Candida spp. were detected 48%, 54.7%, 56%, 21.3%, 18.7%, and 4%, respectively. Methicillin-resistant S. aureus, vancomycin-resistant enterococci and ESBL producing Gram-negative were found 46.8%, 1.3%, and 28.7%, respectively. Pvl, tsst-1, and SEs genes were found in a 2.8/4.9%, 1.4/1.2%, and 100/ 87.8% of the S. aureus/CoNS strains, respectively. The sea gene was found the most common enterotoxigenic gene. blaTEM, blaSHV, blaCTX-M-2, blaCTX-M-1, blaKPC, and blaOXA-48 were found 55.8%, 46.5%, 41.2%, 18.6%, 18.6%, and 18.6%, respectively in Gram-negative strains. CONCLUSIONS: These results is very important to highlight hygienic status of paper currencies. This can be considered as an indication that banknotes may contribute to the spread of pathogens and antimicrobial resistance. Therefore, we may need to start using alternative products instead of banknotes.

Reduced Akkermansia muciniphila and Faecalibacterium prausnitzii levels in the gut microbiota of children with allergic asthma.

INTRODUCTION AND OBJECTIVES: The amounts of Akkermansia muciniphila and Faecalibacterium prausnitzii in gut microbiota are reduced in patients with allergic diseases compared to healthy controls. We aimed to quantify levels of A. muciniphila and F. prausnitzii amounts using real-time quantitative PCR (qPCR) in the gut microbiota of children with allergic asthma and in healthy controls. MATERIALS AND METHODS: In total, 92 children between the ages of three and eight who were diagnosed with asthma and 88 healthy children were included in the study and bacterial DNA was isolated from the stool samples using the stool DNA isolation Kit. qPCR assays were studied with the microbial DNA qPCR Kit for A. muciniphila and microbial DNA qPCR Kit for F. prausnitzii. RESULTS: Both bacterial species showed a reduction in the patient group compared to healthy controls. A. muciniphila and F. prausnitzii were found to be 5.45±0.004, 6.74±0.01 and 5.71±0.002, 7.28±0.009 in the stool samples of the asthma and healthy control groups, respectively. CONCLUSIONS: F. prausnitzii and A. muciniphila may have induced anti-inflammatory cytokine IL-10 and prevented the secretion of pro-inflammatory cytokines like IL-12. These findings suggest that A. muciniphila and F. prausnitzii may suppress inflammation through its secreted metabolites.

The protective role of Helicobacter pylori neutrophil-activating protein in childhood asthma.

BACKGROUND: Helicobacter pylori quantity and HP-NAP gene expression were evaluated in the faeces of healthy and asthmatic children. METHODS: H. pylori DNAs and RNAs were isolated from the stool samples of 92 asthmatic children (AC; 3-8 years) and 88 healthy controls (HC). Quantitative PCR was used to determine the quantity of H. pylori and HP-NAP expression relative to the 16S rRNA (reference gene). Gene expression was analysed using the delta delta-Ct method. RESULTS: H. pylori DNA was detected in the stool samples of 18 (20.4%) of the 88 HC (p<0.0001, OR=0.79) and none of AC. No meaningful statistical differences were found between individuals with positive and negative family histories for asthma in AC and HC (p>0.05). H. pylori quantity was higher in seven of 18 H. pylori-positive samples, but HP-NAP expression levels were low in four of these seven samples. Based on a multivariate logistic regression analysis of these three variables together, only males displayed a significant difference based on gender differences (p<0.02) and it was determined that, based on the OR value of 0.46 and the 95% CI range of 0.241-0.888, male gender was an independent protective factor in asthma. CONCLUSIONS: HP-NAP levels vary to the relative concentrations of bacteria in the stationary or late logarithmic phases. Different napA expression levels may be caused by different endogenous napA gene expression or different environmental conditions.