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Pyrin Gene Polymorphisms and H. pylori-associated Dyspepsia: A Sri Lankan Study

Received: 20 December 2020    Accepted: 11 January 2021    Published: 22 January 2021
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Abstract

Background/Aim: A considerable high number of dyspeptic patients were reported even with the decreasing prevalence of H. pylori in Sri Lanka. Several microbial, host, and environmental factors may associate with the disease outcome. Pyrin secreted by the white blood cells may modulate the inflammatory process by assembling inflammasome complexes in response to pathogen infection. This study focused on the role of pyrin gene polymorphism in gastric mucosal severity and H. pylori infection. Materials and Methods: Among the ninety dyspeptic patients three gastric biopsies were taken and the presence of H. pylori, yeast species and the gastric mucosal severity was determined. EDTA blood was used for DNA extraction and identification of pyrin gene polymorphism. 12 MEFV gene mutations were tested. Results: Most of the patients (61%) had mild chronic gastritis. Among them 11.1% specimens gave positive bands for NL1/LS2 PCR of yeast DNA. H. pylori was positive in 17 patients. No homozygous mutations were found in the MEFV gene. The most common three heterozygous mutations were E148Q (45%), P369S (5%), M680I (11.6%). No significant difference was observed between the presence of the gene polymorphism, gastric mucosal severity or the presence of H. pylori and yeast species in the study group. Conclusion: The absence of homozygous mutations in the MEFV gene suggests that it is not a main factor contributing to gastric mucosal severity. The presence of H. pylori and yeasts reinforce the concept that stomach is a non-sterile environment.

Published in American Journal of Laboratory Medicine (Volume 6, Issue 1)
DOI 10.11648/j.ajlm.20210601.11
Page(s) 1-7
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

H. pylori, Gut Microbiota, Pyrin

References
[1] Nardone G, and Compare D. The human gastric microbiota: Is it time to rethink the pathogenesis of stomach diseases. United European Gastroenterology Journal, 2015; 3 (3): 255-260.
[2] Ianiro G, Molina-Infante J and Gasbarrini A. Gastric Microbiota. Helicobacter. 2015; 20: 68-71.
[3] Von Rosenvinge E, Song Y, White J, Maddox C, Blanchard T and Fricke W. Immune status, antibiotic medication, and pH are associated with changes in the stomach fluid microbiota. The ISME Journal, 2013; 7 (7): 1354-1366.
[4] Lars E, Mathilda L. Helicobacter pylori and the gastric microbiota. Best Practice & Research Clinical Gastroenterology. 2013; 27 (1): 39-45.
[5] Fernando N, Ubhayawardana N, Weerasekera M, Weerasekera D, Samarasinghe K, Gunasekara, C. Detection of clarithromycin-resistant Helicobacter pylori strains in a dyspeptic patient population in Sri Lanka by polymerase chain reaction-restriction fragment length polymorphism. Indian Journal of Medical Microbiology. 2015; 33 (3): 374.
[6] Pereira V, Abraham P, Nallapeta S, Shetty A. Gastric bacterial Flora in patients Harboring Helicobacter pylori with or without chronic dyspepsia: analysis with matrix-assisted laser desorption ionization time-of-flight mass spectroscopy. BMC Gastroenterology 2018; 18 (1):
[7] Han, H, Lee S, Oh S, Moon H, Cho H, Kim J. Correlations of the Gastric and Duodenal Microbiota with Histological, Endoscopic, and Symptomatic Gastritis. Journal of Clinical Medicine. 2019; 8 (3): 312.
[8] Leif Percival Andersen, Susanne Holck, Limas Kupcinskas, Gediminas Kiudelis, Laimas Jonaitis, Dainius Janciauskas, Henrik Permin, Torkel Wadström, Gastric inflammatory markers and interleukins in patients with functional dyspepsia treated with astaxanthin, FEMS Immunology & Medical Microbiology. 2007; 50 (2): 244–248.
[9] Zmora N, Levy M, Pevsner-Fishcer M, Elinav E. Inflammasomes and intestinal inflammation. Mucosal Immunology. 2017; 10 (4): 865-883.
[10] Xu H, Yang J, Gao W, Li L, Li P, Zhang L, Gong Y, Peng X, Xi J, Chen S, Wang F, Shao F. Innate immune sensing of bacterial modifications of Rho GTPases by the Pyrin inflammasome. Nature. 2014; 513 (7517): 237-241.
[11] Stolte M, Meining A. The Updated Sydney System: Classification and Grading of Gastritis as the Basis of Diagnosis and Treatment. Canadian Journal of Gastroenterology. 2001; 15 (9): 591-598.
[12] Ramis IB, de Moraes EP, Fernandes MS, Mendoza-Sassi R, Rodrigues O, Juliano CRV. Evaluation of diagnostic methods for the detection of Helicobacter pylori in gastric biopsy specimens of dyspeptic patients. Brazilian J Microbiol. 2012; 43 (3): 903–8.
[13] Weerasekera M, Sissons C, Wong L, Anderson S, Holmes A, Cannon R. Use of denaturing gradient gel electrophoresis for the identification of mixed oral yeasts in human saliva. Journal of Medical Microbiology. 2013; 62 (2): 319-330.
[14] Bik E, Eckburg P, Gill S, Nelson K, Purdom E, Francois F, Perez-Perez G, Blaser M, Relman D. Molecular analysis of the bacterial microbiota in the human stomach. Proceedings of the National Academy of Sciences. 2006; 103 (3): 732-737.
[15] Gong Y, Zheng J, Jin B, Zhuo D, Huang Z, Qi H, Zhang W, Duan W, Fu J, Wang C, Mao Z, Particular Candida albicans Strains in the Digestive Tract of Dyspeptic Patients, Identified by Multilocus Sequence Typing. PLoS ONE. 2012; 7 (4): e35311.
[16] Darwazeh A, Al-Refai S, Al-Mojaiwel S. Isolation of Candida species from the oral cavity and fingertips of complete denture wearers. The Journal of Prosthetic Dentistry. 2001; 86 (4): 420-423.
[17] Samaranayake L. Commensal Oral Candida in Asian Cohorts. International Journal of Oral Science. 2009; 1 (1): 2-5.
[18] Karczewska E, Wojtas I, Sito E, Trojanowska D, Budak A, Zwolinska-Wcislo M, Wilk A. Assessment of co-existence of Helicobacter pylori and Candida fungi in diseases of the upper gastrointestinal tract. J Physiol Pharmacol. 2009 Dec; 60 Suppl 6: 33-9. PMID: 20224149.
[19] Agin M, Tumgor, G, Kont A, Karakoc G, Altintas D, Yılmaz M, Endoscopic findings in patients with familial Mediterranean fever and dyspeptic symptoms. Gastroenterology Review. 2018; 13 (3): pp. 238-241.
[20] Saikumar C, Manonmoney J. Co-Existence of Helicobacter Pylori and Candida in Upper Gastrointestinal Diseases. Research Journal of Pharmaceutical, Biological and Chemical Sciences. 2014; 749-754.
[21] Tanigawa, T., Watanabe, T., Higuchi, K., Machida, H., Okazaki, H., & Yamagami, H. et al. (2009). Lansoprazole, a Proton Pump Inhibitor, Suppresses Production of Tumor Necrosis Factor-α and Interleukin-1β Induced by Lipopolysaccharide and Helicobacter Pylori Bacterial Components in Human Monocytic Cells via Inhibition of Activation of Nuclear Factor-κB and Extracellular Signal-Regulated Kinase. Journal Of Clinical Biochemistry And Nutrition, 45 (1), 86-92. doi: 10.3164/jcbn.08-267.
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    Yashodha Weerasinghe, Chinthika Gunasekara, Manjula Weerasekera, Surangi Jayakody, Bimalka Seneviratne, et al. (2021). Pyrin Gene Polymorphisms and H. pylori-associated Dyspepsia: A Sri Lankan Study. American Journal of Laboratory Medicine, 6(1), 1-7. https://doi.org/10.11648/j.ajlm.20210601.11

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    ACS Style

    Yashodha Weerasinghe; Chinthika Gunasekara; Manjula Weerasekera; Surangi Jayakody; Bimalka Seneviratne, et al. Pyrin Gene Polymorphisms and H. pylori-associated Dyspepsia: A Sri Lankan Study. Am. J. Lab. Med. 2021, 6(1), 1-7. doi: 10.11648/j.ajlm.20210601.11

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    AMA Style

    Yashodha Weerasinghe, Chinthika Gunasekara, Manjula Weerasekera, Surangi Jayakody, Bimalka Seneviratne, et al. Pyrin Gene Polymorphisms and H. pylori-associated Dyspepsia: A Sri Lankan Study. Am J Lab Med. 2021;6(1):1-7. doi: 10.11648/j.ajlm.20210601.11

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  • @article{10.11648/j.ajlm.20210601.11,
      author = {Yashodha Weerasinghe and Chinthika Gunasekara and Manjula Weerasekera and Surangi Jayakody and Bimalka Seneviratne and Deepaka Weerasekara and Chaturika Jayasinghe and Navoda Perera and Thilini Gamage and Neluka Fernando},
      title = {Pyrin Gene Polymorphisms and H. pylori-associated Dyspepsia: A Sri Lankan Study},
      journal = {American Journal of Laboratory Medicine},
      volume = {6},
      number = {1},
      pages = {1-7},
      doi = {10.11648/j.ajlm.20210601.11},
      url = {https://doi.org/10.11648/j.ajlm.20210601.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajlm.20210601.11},
      abstract = {Background/Aim: A considerable high number of dyspeptic patients were reported even with the decreasing prevalence of H. pylori in Sri Lanka. Several microbial, host, and environmental factors may associate with the disease outcome. Pyrin secreted by the white blood cells may modulate the inflammatory process by assembling inflammasome complexes in response to pathogen infection. This study focused on the role of pyrin gene polymorphism in gastric mucosal severity and H. pylori infection. Materials and Methods: Among the ninety dyspeptic patients three gastric biopsies were taken and the presence of H. pylori, yeast species and the gastric mucosal severity was determined. EDTA blood was used for DNA extraction and identification of pyrin gene polymorphism. 12 MEFV gene mutations were tested. Results: Most of the patients (61%) had mild chronic gastritis. Among them 11.1% specimens gave positive bands for NL1/LS2 PCR of yeast DNA. H. pylori was positive in 17 patients. No homozygous mutations were found in the MEFV gene. The most common three heterozygous mutations were E148Q (45%), P369S (5%), M680I (11.6%). No significant difference was observed between the presence of the gene polymorphism, gastric mucosal severity or the presence of H. pylori and yeast species in the study group. Conclusion: The absence of homozygous mutations in the MEFV gene suggests that it is not a main factor contributing to gastric mucosal severity. The presence of H. pylori and yeasts reinforce the concept that stomach is a non-sterile environment.},
     year = {2021}
    }
    

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  • TY  - JOUR
    T1  - Pyrin Gene Polymorphisms and H. pylori-associated Dyspepsia: A Sri Lankan Study
    AU  - Yashodha Weerasinghe
    AU  - Chinthika Gunasekara
    AU  - Manjula Weerasekera
    AU  - Surangi Jayakody
    AU  - Bimalka Seneviratne
    AU  - Deepaka Weerasekara
    AU  - Chaturika Jayasinghe
    AU  - Navoda Perera
    AU  - Thilini Gamage
    AU  - Neluka Fernando
    Y1  - 2021/01/22
    PY  - 2021
    N1  - https://doi.org/10.11648/j.ajlm.20210601.11
    DO  - 10.11648/j.ajlm.20210601.11
    T2  - American Journal of Laboratory Medicine
    JF  - American Journal of Laboratory Medicine
    JO  - American Journal of Laboratory Medicine
    SP  - 1
    EP  - 7
    PB  - Science Publishing Group
    SN  - 2575-386X
    UR  - https://doi.org/10.11648/j.ajlm.20210601.11
    AB  - Background/Aim: A considerable high number of dyspeptic patients were reported even with the decreasing prevalence of H. pylori in Sri Lanka. Several microbial, host, and environmental factors may associate with the disease outcome. Pyrin secreted by the white blood cells may modulate the inflammatory process by assembling inflammasome complexes in response to pathogen infection. This study focused on the role of pyrin gene polymorphism in gastric mucosal severity and H. pylori infection. Materials and Methods: Among the ninety dyspeptic patients three gastric biopsies were taken and the presence of H. pylori, yeast species and the gastric mucosal severity was determined. EDTA blood was used for DNA extraction and identification of pyrin gene polymorphism. 12 MEFV gene mutations were tested. Results: Most of the patients (61%) had mild chronic gastritis. Among them 11.1% specimens gave positive bands for NL1/LS2 PCR of yeast DNA. H. pylori was positive in 17 patients. No homozygous mutations were found in the MEFV gene. The most common three heterozygous mutations were E148Q (45%), P369S (5%), M680I (11.6%). No significant difference was observed between the presence of the gene polymorphism, gastric mucosal severity or the presence of H. pylori and yeast species in the study group. Conclusion: The absence of homozygous mutations in the MEFV gene suggests that it is not a main factor contributing to gastric mucosal severity. The presence of H. pylori and yeasts reinforce the concept that stomach is a non-sterile environment.
    VL  - 6
    IS  - 1
    ER  - 

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Author Information
  • Department of Microbiology, Faculty of Medical Sciences, University of Sri Jayewardenepura, Gangodawila, Nugegoda, Sri Lanka

  • Department of Microbiology, Faculty of Medical Sciences, University of Sri Jayewardenepura, Gangodawila, Nugegoda, Sri Lanka

  • Department of Microbiology, Faculty of Medical Sciences, University of Sri Jayewardenepura, Gangodawila, Nugegoda, Sri Lanka

  • Department of Community Medicine, Faculty of Medical Sciences, University of Sri Jayewardenepura, Gangodawila, Nugegoda, Sri Lanka

  • Department of Pathology, Faculty of Medical Sciences, University of Sri Jayewardenepura, Gangodawila, Nugegoda, Sri Lanka

  • Department of Surgery, Faculty of Medical Sciences, University of Sri Jayewardenepura, Gangodawila, Nugegoda, Sri Lanka

  • Department of Medical Laboratory Sciences, Faculty of Medical Sciences, University of Sri Jayewardenepura, Gangodawila, Nugegoda, Sri Lanka

  • Department of Medical Laboratory Sciences, Faculty of Medical Sciences, University of Sri Jayewardenepura, Gangodawila, Nugegoda, Sri Lanka

  • Department of Microbiology, Faculty of Medical Sciences, University of Sri Jayewardenepura, Gangodawila, Nugegoda, Sri Lanka

  • Department of Microbiology, Faculty of Medical Sciences, University of Sri Jayewardenepura, Gangodawila, Nugegoda, Sri Lanka

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