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Virulence Markers of Helicobacter Pylori in Patients with Diarrhoea-Dominant Irritable Bowel Syndrome. Javed Yakoob Aga Khan University

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Virulence Markers of Helicobacter Pylori in Patients with Diarrhoea-Dominant Irritable Bowel Syndrome. Javed Yakoob Aga Khan University eCommons@AKU Department of Medicine Department of Medicine May 2012 Virulence markers of Helicobacter pylori in patients with diarrhoea-dominant irritable bowel syndrome. Javed Yakoob Aga Khan University Zaigham Abbas Aga Khan University S. Naz Aga Khan University M. Islam Aga Khan University Waseem Jafri Aga Khan University Follow this and additional works at: https://ecommons.aku.edu/pakistan_fhs_mc_med_med Part of the Digestive System Diseases Commons Recommended Citation Yakoob, J., Abbas, Z., Naz, S., Islam, M., Jafri, W. (2012). Virulence markers of Helicobacter pylori in patients with diarrhoea-dominant irritable bowel syndrome.. British Journal of Biomedical Science, 69(1), 6-10. Available at: https://ecommons.aku.edu/pakistan_fhs_mc_med_med/110 British Journal of Biomedical Science ISSN: 0967-4845 (Print) (Online) Journal homepage: http://www.tandfonline.com/loi/tbbs20 Virulence markers of Helicobacter pylori in patients with diarrhoea-dominant irritable bowel syndrome J. Yakoob, Z. Abbas, S. Naz, M. Islam & W. Jafri To cite this article: J. Yakoob, Z. Abbas, S. Naz, M. Islam & W. Jafri (2012) Virulence markers of Helicobacterpylori in patients with diarrhoea-dominant irritable bowel syndrome, British Journal of Biomedical Science, 69:1, 6-10, DOI: 10.1080/09674845.2012.11669914 To link to this article: https://doi.org/10.1080/09674845.2012.11669914 Published online: 20 Jan 2016. Submit your article to this journal Article views: 11 Citing articles: 4 View citing articles Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=tbbs20 6 ORIGINAL ARTICLE Virulence markers of Helicobacter pylori in patients with diarrhoea-dominant irritable bowel syndrome ABSTRACT J. YAKOOB, Z. ABBAS, S. NAZ, M. ISLAM and W. JAFRI Department of Medicine, The Aga Khan University, Karachi, Pakistan Recent studies suggest that irritable bowel syndrome (IBS) is associated with low-grade inflammation. This study aims to determine the distribution of Helicobacter pylori Accepted: 15 December 2011 cytotoxin-associated gene A (cagA) and vacuolating cytotoxin A (vacA) alleles (e.g., s1 and s2) in patients with diarrhoea-dominant IBS (IBS-D) as the latter causes Introduction vacuolation in colonic epithelial cells in vitro. One hundred and seventy patients meeting Rome III criteria for IBS-D Helicobacter pylori is a highly prevalent Gram-negative (mean age: 40 ±15 years) were enrolled. Gastric biopsy was microaerophilic bacterium. It causes chronic gastric infection assessed histologically and DNA extraction was performed leading to gastritis, peptic ulcer and eventually gastric by polymerase chain reaction (PCR) for H. pylori genus 16S cancer.1–3 H. pylori infection is associated with remodelling of ribosomal DNA (16S rDNA), cagA and vacA allele s1 and s2. gastric mucosal nerves4 and stimulation of mast cells.5,6 In There was no age- or gender-related difference in H. pylori animal models, H. pylori infection increases the neural positivity in IBS-D compared to the control group. responsiveness of smooth muscle.7 H. pylori was positive in 116 (68%) with IBS-D compared to Virulence markers of H. pylori cytotoxin associated gene 88 (55%) in the control group (P=0.01). cagA was positive in (cagA) and vacuolating cytotoxin gene (vacA) are associated 73 (63%) with IBS-D compared to 42 (48%) in the control with different gastroduodenal diseases.8,9 Most H. pylori group (P=0.03). vacA s1 was positive in 61 (53%) with strains secrete a VacA cytotoxin that causes structural and IBS-D compared to 32 (36%) in the control group (P=0.02). functional alterations in epithelial cells and play an cagA s1 was positive in 39 (34%) with IBS-D compared to important role in the pathogenesis of H. pylori-associated 13 (15%) in the control group (P=0.002). gastroduodenal diseases. Mutation of a hydrophobic region near the VacA amino KEY WORDS: cagA. terminus produces a mutant toxin that fails to induce cell Helicobacter pylori. vacuolation with defective functional activity.10 VacA forms Irritable bowel syndrome. anion-selective channels in artificial planar lipid bilayers that vacA alleles. increase the anion permeability of the HeLa cell plasma membrane and determines membrane depolarisation.11 When added to cultured cells, VacA induces vacuolation, local population in children aged 11–15 years is 53.5%.16 an effect potentiated by pre-exposure of the toxin to low pH. In another study where H. pylori infection was established The anion-selective, voltage-dependent pores formed in by rapid urease test and histopathology, cagA-negative artificial membranes are potentiated by acidic conditions.12 H. pylori infection was present in the majority of non-ulcer Pore formation is required both for cell vacuolation and dyspepsia patients; however, cagA was associated with increase of transepithelial conductivity.12 peptic ulcer and gastric carcinoma.17 vacA alleles s1am1 and Purified pH-activated VacA, when added to Caco-2 cell s1bm1 are associated with H. pylori-associated disease and monolayers, demonstrates enterotoxic effect.13 This is time- inflammation.17 and dose-dependent and is saturable.13 Although VacA is The aim of the present study is to determine the produced by H. pylori in the stomach, it may exert an effect distribution of the H. pylori virulence markers cagA and vacA on more distal regions of the intestine. In gastric and small in irritable bowel syndrome with diarrhoea (IBS-D) bowel epithelia, VacA is known to produce acidic ballooning according to the Rome III criteria, compared to the of the endoplasmic reticulum and permeabilisation of the distribution in patients with chronic diarrhoea. cell membrane, independent of the cytopathic effects.14 In children with diarrhoea, a cytotoxin-inducing vacuolation in HEp-2 cells was detected in 19 out of 618 stool Materials and methods specimens, and these resembled those induced by the vacA of H. pylori.15 A total of 330 patients were enrolled in the study, comprising The prevalence of H. pylori seropositivity in the authors’ 170 (52%) with IBS-D and 160 (48%) with chronic diarrhoea. Mean age of the IBS-D group was 41±15 years (range: 16–83; Correspondence to: Dr. Javed Yakoob males: 116, females: 54). Mean age of the 160 patients with Department of Medicine, Aga Khan University Hospital chronic diarrhoea used as controls was 42±14 years (range Stadium Road, Karachi-74800, Pakistan 15–75; males: 106, females: 54). Patients in the control group Email: [email protected] had abdominal pain or discomfort associated with BRITISH JOURNAL OF BIOMEDICAL SCIENCE 2012 69 (1) H. pylori virulence markers in IBS 7 intermittent diarrhoea that did not fulfill the Rome III under low power (x10) and high power (x40) objective criteria for IBS-D. lenses. Patients meeting the Rome III criteria for IBS-D had symptoms for at least three months, with onset at least six Extraction of genomic DNA months previously.18 These patients underwent thorough The extraction of DNA was performed as described history, physical examination, complete blood count, serum previously.20 Briefly, gastric tissue was homogenised in creatinine, electrolytes, stool microscopy, oesophago- 500 µL sterile water and centrifuged at 12,000 xg for 3 min. gastroduodenoscopy (EGD) and colonoscopy. On EGD, Then, 500 µL lysis buffer (100 mmol/L NaCl, 10 mmol/L gastric and duodenal biopsies were taken for H. pylori Tris-HCl [pH 8.0], 25 mmol/L EDTA, 0.5% sodium dodecyl infection, coeliac disease and giardiasis. On colonoscopy, sulphate) and 10 µL proteinase K (10 mg/mL) were added. rectal biopsy was taken for the diagnosis of inflammatory Incubation was carried out at 50˚C for 20 h, followed by bowel disease, microscopic colitis and infective colitis. They phenol-chloroform extraction and ethanol precipitation. also had serology for tissue transglutaminase (TTG) IgA and The resulting pellet was allowed to dissolve in 40 µL TE IgG antibodies for coeliac disease. buffer (10 mmol/L Tris-HCl [pH 7.4], 0.1 mmol/L EDTA Gastric biopsy specimens were used for histopathology for [pH 8.0]) for 20 h at 37˚C. Samples were stored at –20˚C the diagnosis of H. pylori and DNA extraction for the prior to PCR amplification. The DNA content and purity polymerase chain reaction (PCR) to amplify H. pylori genes were determined by measuring the absorbance at 260 nm for ribosomal DNA (rDNA), cagA and vacA alleles s1 and s2. and 280 nm, respectively, using a spectrophotometer Gastritis was graded on a four-point scale of none (grade (Beckman DU-600, USA). 0), mild (grade 1), moderate (grade 2), and severe (grade 3) according to the Sydney guidelines.19 The presence of PCR amplification H. pylori was assessed on haematoxylin and eosin (H&E)- The PCR reaction was performed using extracted DNA as the stained sections. Diagnosis of H. pylori infection was template. Samples that were positive for Helicobacter genus established when PCR for 16S rDNA or a specific PCR for 16S rDNA were subsequently analysed with different H. pylori was positive. primers to detect the cagA, cagA empty site and vacA alleles Exclusion criteria included previous history of peptic ulcer (e.g., s1 and s2 ) (Table 1) which encode potential virulence disease, history of treatment for H. pylori, concurrent or factors in H. pylori.21,22 If cagA was negative, PCR was recent antibiotic use (e.g., metronidazole, clarithromycin, performed to confirm the presence of cagA empty site in amoxicillin, tetracycline, doxycycline and other cagA-negative strains, and to eliminate cases of amplification cephalosporins), histamine-2 receptor blocker or proton failure. Primers used were those described previously.23,24 pump inhibitor therapy, and concurrent infection with Amplification was carried out in a total volume of 50 mL Blastocystis hominis or Giardia lamblia. containing 2 mL 2 mmol dNTPs, 1 mL 50 pmol each forward The study was approved by the institutional ethics review and reverse primer25,26 (synthesised by MWG automatic committee.
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