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    Comparison of new and classical point mutations associated with clarithromycin resistance in Helicobacter pylori strains isolated from dyspeptic patients and their effects on phenotypic clarithromycin resistance
    (Microbiology Soc, 2019) Kocazeybek, Bekir; Sakli, Merve Kutlu; Yuksel, Pelin; Demirci, Mehmet; Caliskan, Reyhan; Sarp, Tevhide Ziver; Saribas, Suat
    Purpose. We aimed to investigate the presence of three recently identified point mutations (A2115G, G2141A and A2144T) of the 23 S rRNA gene and compare them with the three most frequently encountered point mutations (A2142G, A2142C and A2143G) in Helicobacter pylori strains in Turkey. Methodology. A total of 63 patients (mean 47.08 +/- 12.27) were included. The E-test method (for clarithromycin) was used for the clarithromycin antimicrobial susceptibility test of isolated H. pylori strains. Real-time PCR was used to detect the point mutations. Results. A total of 24 out of 63 H. pylori strains (38.1%) were detected as clarithromycin resistant (>0.5 mg l(-1)). The new A2115G (n:6, 25%), A2144T (n: 7, 29.1%) and G2141A, 8 (n: 8, 33.3%) mutations and the classical A2142G (n: 8, 33.3%) and A2143G (n: 11, 45.8%) point mutations were detected in the 24 clarithromycin-resistant strains. The A2144T point mutation had the highest median MIC value (3 mg l(-1)) amongst the new mutations, but the classical mutations (A2142G and A2143G) had the highest median MIC values (256 mg l(-1)) overall. The presence of the A2115G (OR: 31.66), A2144T (OR: 36.92) or G2141A (OR: 28.16) mutations increased the likelihood of clarithromycin resistance in H. pylori strains by 31.66-, 36.92- and 28.16-fold (ORs), respectively, according to the binary logistic regression analysis. Conclusion. We concluded that classical mutations of the 23 S rRNA gene resulted in higher clarithromycin MIC values than new mutations. These new point mutations caused moderate elevations in the MIC values of clarithromycin-resistant H. pylori strains.
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    Helicobacter pylori-miRNA interaction in gastric cancer tissues: First prospective study from Turkey
    (Edizioni Int Srl, 2019) Demiryas, Suleyman; Kocazeybek, Bekir; Demirci, Mehmet; Caliskan, Reyhan; Kepil, Nuray; Uysal, Hayriye Kirkoyun; Dinc, Harika Oyku
    Helicobacter pylori (H. pylori) is involved in the etiology of gastric cancer (GC). miRNAs are short RNAs that regulate gene expression by marking mRNAs for degradation. miRNAs are involved in tumorigenesis, metastasis, and cell proliferation. We aimed to investigate the miRNA expression profiles of tissues from H. pylori Wand (-) GC patients. Forty GC patients, 20 H. pylori Wand 20 H. pylori (-), and a healthy control group were included. The miRNA expression levels were investigated by microarrays and quantitative RT-PCR. We detected 9 upregulated and 4 downregulated miRNAs by microarray. We selected 5 upregulated and 5 downregulated miRNAs for the quantitative RT-PCR assay. The relative fold changes of miRNAs in the cancerous tissue and non-tumor mucosa specimens of H. pylori (+) GC patients for hsa-miR-194 were 4.24- and 3.83-fold higher, respectively, whereas the hsa-miR-145 expression levels were downregulated 0.33-fold and 0.43-fold, respectively, in the same group. The presence of H. pylori significantly upregulated hsa-miR-194 and downregulated hsa-miR-145 expression levels in H. pylofi(+)GC cases, compared to H. pylori (-) GC cases. Regional differences in the virulence of H. pylori strains may also be involved in the up- or downregulation of miRNA expression levels.
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    The Prevalence of Periodontal Pathogenic Bacteria in Atherosclerotic Cardiovascular Disease
    (Clin Lab Publ, 2020) Gode, Safa; Sarp, Tevhide Z.; Saribas, Suat; Ergin, Sevgi; Kasnak, Gokhan; Dinc, Harika O.; Caliskan, Reyhan
    Background: A possible link between periodontal pathogenic bacteria and atherosclerosis may exist based on the inflammatory mechanisms initiated by bacteria found in periodontal lesions. Our aim was to investigate the presence of DNA originating from T. denticola, C. rectus, T. forsythia, and P. gingivalis in the vascular tissue specimens obtained from patients who underwent surgery for arteriosclerotic vascular disease in this study. Methods: A total of 96 patients diagnosed with valvular heart disease due to atherosclerosis and 85 patients with advanced aortic valve stenosis due to rheumatic fever and had undergone aortic valve replacement were included as the study (PG) and the control groups (CG), respectively. Atheroma plaques and vascular tissue specimens were collected from PG and CG during cardiovascular surgical procedures. Revitalization of the lyophilized T. denticola, ATCC 35405; C. rectus, ATCC 33238; P. gingivalis, ATCC 33277 and T. forsythia, ATCC 43037 strains was performed according to the manufacturer's instructions. C. rectus, T. forsythia, and T. denticola DNA samples were analyzed using the one-step in-house PCR method. Results: In one (1.04%) and three (3.13%) out of 96 atherosclerotic PG tissue specimens, P. gingivalis and T. forsythia DNA were detected, respectively. No T. denticola or C. rectus DNA was found in the study specimens. Periodontal pathogenic bacteria were not observed in 85 CG tissue specimens. There was no statistically significant difference between PG and CG for the presence of P. gingivalis and T. forsythia DNA using Fischer's Exact test (p > 0.05). Conclusions: In conclusion, with the case-control studies on a small scale such as in our study, it is not possible to determine a causality relationship between periodontal pathogenic bacteria and formation of atherosclerosis. Periodontal pathogenic bacteria may not be the only factor that causes inflammatory diseases associated with atherosclerosis. Host response and inflammatory mechanisms may be affected by other factors such as ethnicity, dietary habits, nutritional availability, and lifestyle. Taken together, it is difficult to conclude a causal link between periodontal pathogenic bacteria and formation of atherosclerosis.