Observational Study
Copyright ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 14, 2022; 28(2): 242-262
Published online Jan 14, 2022. doi: 10.3748/wjg.v28.i2.242
Identification of functional tumor necrosis factor-alpha promoter variants associated with Helicobacter pylori infection in the Sudanese population: Computational approach
Abeer Babiker Idris, Alaa B Idris, Manal A Gumaa, Mohammed Babiker Idris, Amanda Elgoraish, Mohamed Mansour, Dalia Allam, Bashir MO Arbab, Nazar Beirag, El-Amin M Ibrahim, Mohamed A Hassan
Abeer Babiker Idris, Department of Agricultural Science and Technology, Institute of Natural and Applied Sciences, Erciyes University, Kayseri 38039, Turkey
Abeer Babiker Idris, Department of Medical Microbiology, Faculty of Medical Laboratory Sciences, University of Khartoum, Khartoum 11111, Sudan. abeer.babiker89@gmail.com
Alaa B Idris, Department of Neurosurgery, Ribat University Hospital, Khartoum 11111, Sudan
Manal A Gumaa, El-Amin M Ibrahim, Department of Medical Microbiology, Faculty of Medical Laboratory Sciences, University of Khartoum, Khartoum 11111, Sudan
Mohammed Babiker Idris, BioMérieux Clinical and Application Advisor, Al-Jeel Medical Co., Riyadh 11422, Saudi Arabia
Amanda Elgoraish, Department of Epidemiology, Tropical Medicine Research Institute, Khartoum 11111, Sudan
Mohamed Mansour, Dalia Allam, Department of Gastroenterology, Ibn Sina Specialized Hospital, Khartoum 11111, Sudan
Bashir MO Arbab, Department of Gastroenterology, Modern Medical Centre, Khartoum 11111, Sudan
Nazar Beirag, Biosciences, College of Health, Medicine and Life Sciences, Brunel University, London UB8 3PH, Uxbridge, United Kingdom
Mohamed A Hassan, Department of Bioinformatics, Africa city of technology, Khartoum 11111, Sudan
Mohamed A Hassan, Department of Bioinformatics, DETAGEN Genetic Diagnostics Center, Kayseri 38350, Turkey
Mohamed A Hassan, Department of Translation Bioinformatics, Detavax Biotech, Kayseri 38350, Turkey
Author contributions: Idris AB and Hassan MA conceptualized and designed the study; Idris AB, Idris A, Gumaa MA, Idris MB, Mansour M, Allam D and Arbab MOB participated in sample collection and analysis of the data; Idris AB and Elgoraish A statistically analyzed the data; Idris AB performed the bioinformatics analysis, interpretation of the data and drafting the article; Idris AB, Beirag N, Mansour M, Hassan MA and Ibrahim EM revised the manuscript’s language and critically assessed the intellectual content; all authors approved the final version of the article to be published.
Institutional review board statement: The study was reviewed and approved by the Khartoum Ministry of Health research department, University of Khartoum, Faculty of Medical Laboratory Sciences review board, and Research Ethics Committees of hospitals.
Informed consent statement: Written informed consent was taken from participants before they enrolled in the study.
Conflict-of-interest statement: The authors declare that there are no conflicts of interest.
Data sharing statement: The data regarding TNF-A-1030 T>C genotypes and alleles distributions among participants and the in silico results of the software that used to support the findings of this study are available from the corresponding author at abeer.babiker89@gmail.com on a reasonable request.
STROBE statement: The authors have read the STROBE Statement-checklist of items, and the manuscript was prepared and revised according to the STROBE Statement-checklist of items.
Corresponding author: Abeer Babiker Idris, DSc, Academic Research, Department of Agricultural Science and Technology, Institute of Natural and Applied Sciences, Erciyes University, Merkez Kampüs Talas Yolu Melikgazi, Kayseri 38039, Turkey. abeer.babiker89@gmail.com
Received: April 29, 2021
Peer-review started: April 29, 2021
First decision: June 17, 2021
Revised: July 13, 2021
Accepted: December 31, 2021
Article in press: December 31, 2021
Published online: January 14, 2022
Processing time: 257 Days and 7.5 Hours
ARTICLE HIGHLIGHTS
Research background

Helicobacter pylori (H. pylori) infection represents a major public health challenge in Sudan. However, functional polymorphisms within the tumor necrosis factor-alpha (TNF-A) promoter are associated with the incidence and progression of H. pylori infection by increasing TNF-α production.

Research motivation

TNF lies within the major histocompatibility complex region of chromosome 6, which is a highly polymorphic region. Therefore, many polymorphisms have been detected in the TNF-A promoter and studying which variants could affect TNF-A gene expression is relevant. However, the influence of these single nucleotide polymorphisms (SNPs) on TNF-α production is not fully known and still a contradictory topic of debate due to the ethnic differences between populations. Furthermore, to our knowledge, there are no previous studies in Sudan that have addressed the association between TNF-A and H. pylori infection or H. pylori-associated diseases.

Research objectives

To functionally characterize the genetic variations in the TNF-A 5’-region (-584 to +107) of Sudanese patients infected with H. pylori and predict if these SNPs could alter the regulatory motifs using bioinformatics analyses. Also, to investigate the mammalian conservation of these SNPs using comparative profiling analysis in 11 species.

Research methods

An observational study was conducted in the major hospitals in Khartoum state. Genomic DNA was extracted from 122 gastric biopsies of patients who had been referred for endoscopy. Genotyping of the TNF-A-1030 polymorphism was performed using PCR with confronting two-pair primer to investigate its association with H. pylori infection in the Sudanese population. Sanger sequencing was applied to detect SNPs in the 5’-region (-584 to +107) of TNF-A in H. pylori-infected patients; in silico tools were used to predict whether these mutations would alter transcription factor binding sites or composite regulatory elements in this region. In addition, the ECR browser and multiple-sequence local alignment and visualization search engine were used to study the conservation of the detected SNPs among 11 mammalian species.

Research results

A total of seven SNPs were observed in the TNF-A 5’-region of Sudanese patients infected with H. pylori. Among them, the SNP (T>A, -76) was located at the in silico-predicted promoter region (-146 to +10), and it was predicted to alter transcription factor binding sites and composite regulatory elements, while the novel mutation (A>T, +27) was detected in the 5’ untranslated region. It could affect the post-transcriptional regulatory pathways. Mammalian conservation was detected for the (-146 to +10) region in chimpanzee (99.4%), rhesus monkey (95.6%), cow (91.8%), domesticated dog (89.3%), mouse (84.3%), rat (82.4%) and opossum (78.0%). Furthermore, genotyping of TNF-A-1030 revealed a lack of significant association between -1030T and susceptibility to H. pylori and gastric cancer in the studied population (P = 0.1756 and P = 0.8116, respectively).

Research conclusions

Despite the high level of genetic variation in the TNF-A 5’-region (-584 to +107) of the Sudanese patients, the sequences involved in enhanceosome formation and gene regulation are highly conserved. Remarkably, only a single SNP (-76) was detected in this region. In addition, computational analysis was a valuable method for studying gene expression patterns and insights for further in vitro and in vivo experimental proofs.

Research perspectives

Further large cohort studies are needed to assess the association between (T>A, -76) mutation and H. pylori infection (susceptibility and progression). Also, further studies are encouraged to investigate the novel mutation (A>T, +27) in terms of the frequency of the minor allele (T) in the Sudanese population and its functional significance using computational and experimental approaches. Identifying which of these detected variants are functional is of great relevance for discovering new preventive, diagnostic and therapeutic strategies against the incidence and/or progression of multifactorial diseases such as H. pylori infection.