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Hussein NR, Tunjel I, Majed HS, et al. Duodenal ulcer promoting gene 1 (dupA1) is associated with A2147G clarithromycin-resistance mutation but not interleukin-8 secretion from gastric mucosa in Iraqi patients. New Microbes New Infect. 2015;6:5-10doi: 10.1016/j.nmni.2015.02.005.
Hussein, N. R., Tunjel, I., Majed, H. S., Yousif, S. T., Aswad, S. I., & Assafi, M. S. (2015). Duodenal ulcer promoting gene 1 (dupA1) is associated with A2147G clarithromycin-resistance mutation but not interleukin-8 secretion from gastric mucosa in Iraqi patients. New microbes and new infections, 65-10. https://doi.org/10.1016/j.nmni.2015.02.005
Hussein, N R, et al. "Duodenal ulcer promoting gene 1 (dupA1) is associated with A2147G clarithromycin-resistance mutation but not interleukin-8 secretion from gastric mucosa in Iraqi patients." New microbes and new infections vol. 6 (2015): 5-10. doi: https://doi.org/10.1016/j.nmni.2015.02.005
Hussein NR, Tunjel I, Majed HS, Yousif ST, Aswad SI, Assafi MS. Duodenal ulcer promoting gene 1 (dupA1) is associated with A2147G clarithromycin-resistance mutation but not interleukin-8 secretion from gastric mucosa in Iraqi patients. New Microbes New Infect. 2015 Mar 04;6:5-10. doi: 10.1016/j.nmni.2015.02.005. eCollection 2015 Jul. PMID: 26042186; PMCID: PMC4442689.
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New Microbes New Infect. 2015 Mar 04;6:5-10. doi: 10.1016/j.nmni.2015.02.005. eCollection 2015 Jul.

Duodenal ulcer promoting gene 1 (dupA1) is associated with A2147G clarithromycin-resistance mutation but not interleukin-8 secretion from gastric mucosa in Iraqi patients.

New microbes and new infections

N R Hussein, I Tunjel, H S Majed, S T Yousif, S I Aswad, M S Assafi

Affiliations

  1. Department of Internal Medicine, The School of Medical Sciences, Faculty of Medicine, University of Duhok, Kurdistan Region, Iraq.
  2. Department of Biology, Faculty of Science, Fatih University, Istanbul, Turkey.
  3. Nutrition Unit, Duhok Diabetes Centre, Duhok, Kurdistan Region, Iraq.
  4. Department of Biology, Faculty of Sciences, University of Zakho, Kurdistan Region, Iraq.

PMID: 26042186 PMCID: PMC4442689 DOI: 10.1016/j.nmni.2015.02.005

Abstract

Helicobacter pylori causes peptic ulceration and gastric adenocarcinoma. The aims were to study the influence of dupA1 positivity upon interleukin-8 (IL-8) secretion from gastric mucosa and determine the prevalence of mutations responsible for clarithromycin and fluoroquinolone resistance. DNA was extracted from 74 biopsies and the virulence factors were studied. Levels of IL-8 in gastric mucosa were measured using ELISA and the mutations responsible for clarithromycin and fluoroquinolone resistance were determined using a GenoType-HelicoDR assay. The prevalence of cagA in strains isolated from gastric ulcer (GU) and duodenal ulcer (DU) was significantly higher than those isolated from non-ulcer disease (NUD) (90% and 57.9% versus 33.3%; p 0.01). The vacA s1m1 genotype was more prevalent in patients with DU (73.7%) and GU (70%) than in those with NUD (13.3%) (p 0.01). The prevalence of dupA1 was higher in DU patients (36.8%) than those with GU (10%) and NUD (8.9%) (p 0.01). Multivariate analysis showed that a cagA+/vacA s1i1m2 virulence gene combination was independently associated with the developing peptic ulcer disease (PUD) with increased odds of developing PUD (p 0.03; OR = 2.1). We found no significant difference in the levels of IL-8 secretion in gastric mucosa infected with H. pylori dupA-negative and H. pylori dupA1-positive strains (dupA-negative: mean ± median: 28 ± 26 versus 30 ± 27.1 for dupA1; p 0.6). While 12 strains were clarithromycin resistant, only three isolates were levofloxacin resistant. A significant association was found between dupA1 genotype and A2147G clarithromycin resistance mutation (p <0.01). Further study is needed to explore the relationship between virulence factors and disease process and treatment failure.

Keywords: Antibiotic sensitivity; Iraq; clarithromycin; dupA; fluoroquinolones

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