Differential expression of miRNA-146a and miRNA-155 in gastritis induced by  Helicobacter pylori  infection in paediatric patients, adults, and an animal model

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Abstract

Background

Helicobacter pylori is a major aetiologic agent associated with gastritis. H. pylori infections increase the expression of the Toll-like receptor (TLR), which in turn modulates the expression of microRNA (miRNA)-146a and miRNA-155. The objective of this study was to compare the expression of miRNA-146a and miRNA-155 in gastric lesions of paediatric and adult patients with different pathologies and in Mongolian gerbils ( Meriones unguiculatus) infected with H. pylori 26,695.

Methods

Quantification of miRNA expression was performed by quantitative real-time polymerase chain reaction (qRT-PCR) of paraffin-embedded gastric lesions of children with or without an infection ( n = 25), adults with follicular gastritis and metaplasia ( n = 32) and eight-week-old M. unguiculatus males (Hsd:MON) infected with H. pylori 26,695 for 0, 3, 6, 12 and 18 months (n = 25). The genes RNU48 and RNU6 were used as endogenous controls for data normalization. Statistical analyses were performed using Kruskal-Wallis, Mann-Whitney, ANOVA and Student’s t-test.

Results

The expression of miRNA-146a and miRNA-155 in infected children increased by 247.6- and 79.4-fold (on average), respectively, compared to that observed in the control group. However, these results were not significant ( p = 0.12 and p = 0.07 respectively). In some children a gradual increase in expression was observed, while in others, expression was very high. Additionally, the expression levels of miRNA-146a and miRNA-155 increased by an average of 21.7- and 62-fold, respectively, in adult patients with follicular gastritis when compared to those of the controls. In M. unguiculatus infected with H. pylori 26,695, the expression of both miRNAs increased as the infection progressed.

Conclusion

This is the first report to show differences in the expression of miRNA-146a and miRNA-155 in paediatric and adult patients with gastritis who were infected with H. pylori. In addition, in M. unguiculatus infected with H. pylori, miRNA expression was associated with the progression of infection and the ability of the bacteria to adapt to the host.

Electronic supplementary material

The online version of this article (10.1186/s12879-018-3368-2) contains supplementary material, which is available to authorized users.

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Most cited references 27

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Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994.

M F Dixon, R M Genta, J Yardley … (1996)

The Sydney System for the classification of gastritis emphasized the importance of combining topographical, morphological, and etiological information into a schema that would help to generate reproducible and clinically useful diagnoses. To reappraise the Sydney System 4 years after its introduction, a group of gastrointestinal pathologists from various parts of the world met in Houston, Texas, in September 1994. The aims of the workshop were (a) to establish an agreed terminology of gastritis; (b) to identify, define, and attempt to resolve some of the problems associated with the Sydney System. This article introduces the Sydney System as it was revised at the Houston Gastritis Workshop and represents the consensus of the participants. Overall, the principles and grading of the Sydney System were only slightly modified, the grading being aided by the provision of a visual analogue scale. The terminology of the final classification has been improved to emphasize the distinction between the atrophic and nonatrophic stomach; the names used for each entity were selected because they are generally acceptable to both pathologists and gastroenterologists. In addition to the main categories and atrophic and nonatrophic gastritis, the special or distinctive forms are described and their respective diagnostic criteria are provided. The article includes practical guidelines for optimal biopsy sampling of the stomach, for the use of the visual analogue scales for grading the histopathologic features, and for the formulation of a comprehensive standardized diagnosis. A glossary of gastritis-related terms as used in this article is provided.

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The kinase Akt1 controls macrophage response to lipopolysaccharide by regulating microRNAs.

Ariadne Androulidaki, Dimitrios Iliopoulos, Alicia Arranz … (2009)

MicroRNAs regulated by lipopolysaccharide (LPS) target genes that contribute to the inflammatory phenotype. Here, we showed that the protein kinase Akt1, which is activated by LPS, positively regulated miRNAs let-7e and miR-181c but negatively regulated miR-155 and miR-125b. In silico analyses and transfection studies revealed that let-7e repressed Toll-like receptor 4 (TLR4), whereas miR-155 repressed SOCS1, two proteins critical for LPS-driven TLR signaling, which regulate endotoxin sensitivity and tolerance. As a result, Akt1(-/-) macrophages exhibited increased responsiveness to LPS in culture and Akt1(-/-) mice did not develop endotoxin tolerance in vivo. Overexpression of let-7e and suppression of miR-155 in Akt1(-/-) macrophages restored sensitivity and tolerance to LPS in culture and in animals. These results indicate that Akt1 regulates the response of macrophages to LPS by controlling miRNA expression.

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MicroRNAs are differentially expressed in ulcerative colitis and alter expression of macrophage inflammatory peptide-2 alpha.

Feng Dan Wu, Michelle N Zikusoka, Anil Trindade … (2008)

Chronic inflammatory bowel diseases such as ulcerative colitis (UC) are associated with differential expression of genes involved in inflammation and tissue remodeling. MicroRNAs (miRNAs), which direct mRNA degradation and translational inhibition, influence a number of disease processes. We examined whether miRNAs are differentially expressed in UC tissues and are associated with expression of genes that regulate inflammation. miRNA expression was assessed in patients with active UC, inactive UC, Crohn's disease, irritable bowel syndrome, infectious colitis, and microscopic colitis, as well as in healthy subjects by microarray, quantitative reverse transcription-polymerase chain reaction and in situ hybridization analyses. Colonic epithelial cell (HT29) expression of miRNAs was assessed. Regulation of gene expression by miRNAs was assessed by luciferase reporter construct assays and transfection of specific miRNA mimics. Active UC was associated with the differential expression of 11 miRNAs; 3 were significantly decreased and 8 were significantly increased in UC tissues. In situ hybridization analysis indicated that miR-192, an miRNA with decreased expression in active UC, was predominantly localized to colonic epithelial cells. Macrophage inflammatory peptide (MIP)-2 alpha, a chemokine expressed by epithelial cells, was identified as a target of miR-192. In colon epithelial cells, induction of MIP-2 alpha expression by tumor necrosis factor-alpha was accompanied by a concomitant reduction in miR-192 expression and miR-192 was observed to regulate the expression of MIP-2 alpha. These findings expand the known roles of miRNAs, indicating that tissues from patients with UC, and possibly other chronic inflammatory diseases, have altered miRNA expression patterns. These findings also demonstrate that miRNAs regulate colonic epithelial cell-derived chemokine expression.

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Author and article information

Contributors

Ana Caren Cortés-Márquez: yurico_cts@hotmail.com

Sandra Mendoza-Elizalde: smendoza@himfg.edu.mx

Francisco Arenas-Huertero: farenashuertero@yahoo.com.mx

Jimena Trillo-Tinoco: Jimena.Trillo-Tinoco@moffitt.org

Pedro Valencia-Mayoral: pvalencia@himfg.edu.mx

Alejandra Consuelo-Sánchez: draalejandraconsuelo@yahoo.com.mx

Jonathan Zarate-Franco: thelostpondjurasicduck@hotmail.com

Ada Ruth Dionicio-Avendaño: ruthavenda_o@yahoo.com.mx

José de Jesús Herrera-Esquivel: josehe_3@yahoo.com.mx

Elio Germán Recinos-Carrera: grecinosc@yahoo.com.mx

Christian Colín-Valverde: metallicaifanes@hotmail.com

Sandra Rivera-Gutiérrez: san_rg@yahoo.com.mx

Juan Carlos Vigueras-Galindo: jcvazul@yahoo.com

Norma Velázquez-Guadarrama: normave@himfg.edu.mx

Journal

Journal ID (nlm-ta): BMC Infect Dis

Journal ID (iso-abbrev): BMC Infect. Dis

Title: BMC Infectious Diseases

Publisher: BioMed Central (London )

ISSN (Electronic): 1471-2334

Publication date (Electronic): 15 September 2018

Publication date PMC-release: 15 September 2018

Publication date Collection: 2018

Volume: 18

Electronic Location Identifier: 463

Affiliations

[1 ]ISNI 0000 0004 0633 3412, GRID grid.414757.4, Infectology Laboratory, , Hospital Infantil de México Federico Gómez, ; México City, Mexico

[2 ]ISNI 0000 0001 2165 8782, GRID grid.418275.d, Biomedicine and Molecular Biotechnology, Escuela Nacional de Ciencias Biológicas, , Instituto Politécnico Nacional, ; México City, Mexico

[3 ]ISNI 0000 0001 2165 8782, GRID grid.418275.d, Molecular Microbiology Laboratory, Microbiology Department, Escuela Nacional de Ciencias Biológicas, , Instituto Politécnico Nacional, ; México City, Mexico

[4 ]ISNI 0000 0004 0633 3412, GRID grid.414757.4, Laboratory of Research in Experimental Pathology, , Hospital Infantil de México Federico Gómez, ; México City, Mexico

[5 ]ISNI 0000 0000 9891 5233, GRID grid.468198.a, Department of Immunology, , Moffitt Cancer Center, ; Tampa, FL USA

[6 ]ISNI 0000 0004 0633 3412, GRID grid.414757.4, Planning Direction, , Hospital Infantil de México Federico Gómez, ; México City, Mexico

[7 ]ISNI 0000 0004 0633 3412, GRID grid.414757.4, Gastroenterology and Nutrition Department, , Hospital Infantil de México Federico Gómez, ; México City, Mexico

[8 ]ISNI 0000 0001 2165 8782, GRID grid.418275.d, Health Science, Escuela Superior de Medicina, , Instituto Politécnico Nacional, ; México City, Mexico

[9 ]Endoscopy Department, Hopital General Dr. Manuel Gea González, México City, Mexico

[10 ]GRID grid.414754.7, Division of Pathological Anatomy, , Hospital General Dr. Manuel Gea González, ; México City, Mexico

[11 ]ISNI 0000 0004 0633 3412, GRID grid.414757.4, Center of Economic and Social Studies in Health, , Hospital Infantil de México Federico Gómez, ; México City, Mexico

Article

Publisher ID: 3368

DOI: 10.1186/s12879-018-3368-2

PMC ID: 6139157

PubMed ID: 30219037

SO-VID: 1b1eee13-2b04-42ee-a449-c0d09c589941

License:

Open AccessThis article is 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, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 19 January 2018

Date accepted : 30 August 2018

Funding

Funded by: Federal Resources. Ministry of Health and Assistance (SSA), México

Award ID: HIM/2013/009.SSA 1081

Funded by: Federal Ministry of Health and Assistance (SSA), México

Award ID: HIM/2011/080-SSA 1005

Custom metadata

ScienceOpen disciplines: Infectious disease & Microbiology

Keywords: helicobacter pylori,gastritis,mirna-146a,mirna-155,meriones unguiculatus

Data availability:

ScienceOpen disciplines: Infectious disease & Microbiology

Keywords: helicobacter pylori, gastritis, mirna-146a, mirna-155, meriones unguiculatus

Differential expression of miRNA-146a and miRNA-155 in gastritis induced by Helicobacter pylori infection in paediatric patients, adults, and an animal model

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Abstract

Background

Methods

Results

Conclusion

Electronic supplementary material

Related collections

When did Helicobacter first colonise humans?

Most cited references 27

Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994.

The kinase Akt1 controls macrophage response to lipopolysaccharide by regulating microRNAs.

MicroRNAs are differentially expressed in ulcerative colitis and alter expression of macrophage inflammatory peptide-2 alpha.

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