In developing countries, clarithromycin resistance and frequency of re-infection are factors that contribute to high prevalence of Helicobacter pylori infection. The aim of this research was determine the prevalence of clarithromycin resistance and its relation with A2142G, A2142C and A2143G mutations in the domain V of the 23S rRNA gene of H. pylori isolates in patients from Southern Mexico with chronic gastritis. Another purpose of this work was to study the prevalence of virulent genotypes and distribution of resistant strains according to the vacA/cagA/babA2 H. pylori genotypes. One hundred forty-four patients with chronic gastritis were studied. Forty-five H. pylori strains were isolated and clarithromycin susceptibility was determined by the disk-diffusion method. The 82.2% of the strains had the combination of alleles vacA s1 m1 and the cagA gene was detected in 77.8% and 40% of the strains were babA2 positive. The vacA s1 m1 genotype was detected more frequently in cagA(+) strains, vacA s1m1/cagA(+)/babA2(-) genotype was more frequent than vacA s1m1/cagA(+)/babA2(+), 37.8% and 33.3%, respectively. Eight strains were clarithromycin resistant, in three of these, point mutations were identified, but only in one strain the A2143G mutation associated with clarithromycin resistance was found. Other point mutations (A1821G, G1826A, T1830C, A2089G, T1600C, C1601T, C1602T, T1610C, A1611C and T1633G) that have not been associated with clarithromycin resistance were identified. The highest proportion of resistant strains was vacA s1m1/cagA(+) (62.5%). In patients from southern Mexico with chronic gastritis, the prevalence of clarithromycin resistance is within internationally accepted range (17.8%) and allows continued use of triple therapy for H. pylori eradication. However, it is necessary to monitor the evolution of clarithromycin resistance in this area. The largest proportion of resistant H. pylori strains is not harboring the A2142G, A2142C and A2143G mutations in the 23S rRNA gene (87.5%). The vacA s1m1/cagA(+) genotype was the most prevalent and among clarithromycin-resistant strains, this was the predominant.

PurposeVirulent genotypes of Helicobacter pylori vacA s1m1/cagA+/babA2+ have been associated with severe gastric diseases. VacA, CagA and BabA are polymorphic proteins, and their association with the disease is allele-dependent. The aims of this work were: (i) to determine the prevalence of H. pylori by type of chronic gastritis; (ii) to describe the frequency of cagA, babA2 and vacA genotypes in strains from patients with different types of chronic gastritis; (iii) to characterize the variable region of cagA alleles.MethodologyA total of 164 patients with chronic gastritis were studied. Altogether, 50 H. pylori strains were isolated, and the status of cagA, babA2 and vacA genotypes was examined by PCR. cagA EPIYA segment identification was performed using PCR and sequencing of cagA fragments of six randomly selected strains.Results/Key findingsThe overall prevalence of H. pylori was 30.5 %. Eighty percent of the isolated strains were vacA s1m1, and the cagA and babA2 genes were detected in 74 and 32 % of the strains, respectively. The most frequent genotypes were vacA s1m1/cagA+/babA2- and vacA s1m1/cagA+/babA2+, with 40 % (20/50) and 28 % (14/50), respectively. In cagA+, the most frequent EPIYA motif was -ABC (78.4 %), and EPIYA-ABCC and -ABCCC motifs were found in 10.8 % of the strains. A modified EPIYT-B motif was found in 66.6 % of the sequenced strains.ConclusionH. pylori strains carrying vacA s1m1, cagA+ and babA2- genotypes were the most prevalent in patients with chronic gastritis from the south of Mexico. In the cagA+ strains, the EPIYA-ABC motif was the most common.

Gastrokine 1 (GKN1) is a protein expressed on the surface mucosa cells of the gastric antrum and fundus, which contributes to maintaining gastric homeostasis, inhibits inflammation and is a tumor suppressor. The expression of GKN1 decreases in mucosa that are either inflamed or infected by Helicobacter pylori, and is absent in gastric cancer. The measurement of circulating GKN1 concentration, the protein itself, or the mRNA in gastric tissue may be of use for the early diagnosis of cancer. The mechanisms that modulate the deregulation or silencing of GKN1 expression have not been completely described. The modification of histones, methylation of the GKN1 promoter, or proteasomal degradation of the protein have been detected in some patients; however, these mechanisms do not completely explain the absence of GKN1 or the reduction in GKN1 levels. Only NKX6.3 transcription factor has been shown to be a positive modulator of GKN1 transcription, although others also have an affinity with sequences in the promoter of this gene. While microRNAs (miRNAs) are able to directly or indirectly regulate the expression of genes at the post-transcriptional level, the involvement of miRNAs in the regulation of GKN1 has not been reported. The present review analyzes the information reported on the determination of GKN1 expression and the regulation of its expression at the transcriptional, post-transcriptional and post-translational levels; it proposes an integrated model that incorporates the regulation of GKN1 expression via transcription factors and miRNAs in H. pylori infection.

The overexpression of miR-218-5p in cervical cancer (CC) cell lines decreases migration, invasion and proliferation. The objective was to identify target genes of miR-218-5p and the signaling pathways and cellular processes that they regulate. The relationship between the expression of miR-218-5p and RUNX2 and overall survival in CC as well as the effect of the exogenous overexpression of miR-218-5p on the level of RUNX2 were analyzed. The target gene prediction of miR-218-5p was performed in TargetScan, miRTarBase and miRDB. Predicted target genes were subjected to gene ontology (GO) and pathway enrichment analysis using the Kyoto Encyclopaedia of Genes and Genomes (KEGG). The miR-218-5p mimetic was transfected into C-33A and CaSki cells, and the miR-218-5p and RUNX2 levels were determined by RT–qPCR. Of the 118 predicted targets for miR-218-5p, 86 are involved in protein binding, and 10, including RUNX2, are involved in the upregulation of proliferation. Low miR-218-5p expression and a high level of RUNX2 are related to poor prognosis in CC. miR-218-5p overexpression is related to decreased RUNX2 expression in C-33A and CaSki cells. miR-218-5p may regulate RUNX2, and both molecules may be prognostic markers in CC.

In women, serum levels of CTSB, GKN2, LIPF, LIPFG, AZGP1, TOP2A and PGA4 are proposed as predictive markers of gastric cancer. It is unknown whether GKN1 expression varies with the sex of patients with chronic gastritis or gastric cancer. We studied 36 patients with histopathological diagnosis of chronic gastritis from the state of Guerrero, Mexico. PCR was performed for H. pylori detection and GKN1 expression was determined by RT-qPCR and western blot. GKN1 mRNA expression was significantly lower in patients with chronic follicular gastritis than in those with chronic chemical gastritis (p = 0.00071). The mRNA and protein level of expression of GKN1 were significantly lower in women with chronic follicular gastritis than in men with the same condition (p = 0.0279 and p = 0.0014, respectively); the lowest levels of GKN1 were detected in women with H. pylori-positive follicular gastritis (p = 0.0175 and p = 0.0111, respectively). Through a bioinformatic analysis, estrogen response elements were identified in the GKN1 promoter.