A novel biallelic 19-bp deletion in the IL10RB gene caused infant-onset inflammatory bowel disease in a consanguineous family: a molecular docking simulation study and literature review.

IL10RB gene Inflammatory bowel diseases Iran Mutation Whole exome sequencing

Journal

Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234

Informations de publication

Date de publication:
28 Jan 2024
Historique:
received: 26 11 2023
accepted: 11 01 2024
medline: 28 1 2024
pubmed: 28 1 2024
entrez: 28 1 2024
Statut: epublish

Résumé

Infantile-onset inflammatory bowel disease (IOIBD) is a gastrointestinal inflammatory condition often associated with monogenic disorders and is frequently caused by Interleukin-10 deficiencies. This study aimed to identify the mutation responsible for IBD in an 8-year-old patient from an Iranian family with consanguineous parents. Whole-exome sequencing (WES) was employed to identify disease-causing variations. Furthermore, we utilized integrated experimental data of HADDOCK molecular docking platform, including NMR spectroscopy, to characterize the mutant protein and elucidate the underlying functional mechanism of the identified mutation's pathogenicity. Our findings revealed a novel 19-bp deletion mutation (c.25_43del, p.Leu9CysfsTer15) in the IL10RB gene. Sanger sequencing confirmed that this variant was inherited in homozygous state within this family, marking the first mutation identified in exon 1 of this gene. Molecular docking simulation demonstrated that the mutant form of IL10RB exhibited reduced affinity for binding to the Interleukin-10 ligand, leading to disruptions in downstream cellular signaling pathways. The identification of this novel genetic variant as a causative factor for IOIBD highlights the clinical value of utilizing genetic testing, such as WES, as a reliable diagnostic approach for patients affected by this condition.

Sections du résumé

BACKGROUND BACKGROUND
Infantile-onset inflammatory bowel disease (IOIBD) is a gastrointestinal inflammatory condition often associated with monogenic disorders and is frequently caused by Interleukin-10 deficiencies. This study aimed to identify the mutation responsible for IBD in an 8-year-old patient from an Iranian family with consanguineous parents.
METHODS METHODS
Whole-exome sequencing (WES) was employed to identify disease-causing variations. Furthermore, we utilized integrated experimental data of HADDOCK molecular docking platform, including NMR spectroscopy, to characterize the mutant protein and elucidate the underlying functional mechanism of the identified mutation's pathogenicity.
RESULTS RESULTS
Our findings revealed a novel 19-bp deletion mutation (c.25_43del, p.Leu9CysfsTer15) in the IL10RB gene. Sanger sequencing confirmed that this variant was inherited in homozygous state within this family, marking the first mutation identified in exon 1 of this gene. Molecular docking simulation demonstrated that the mutant form of IL10RB exhibited reduced affinity for binding to the Interleukin-10 ligand, leading to disruptions in downstream cellular signaling pathways.
CONCLUSIONS CONCLUSIONS
The identification of this novel genetic variant as a causative factor for IOIBD highlights the clinical value of utilizing genetic testing, such as WES, as a reliable diagnostic approach for patients affected by this condition.

Identifiants

pubmed: 38281300
doi: 10.1007/s11033-024-09248-4
pii: 10.1007/s11033-024-09248-4
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

223

Subventions

Organisme : Golestan University of Medical Sciences
ID : 113339

Informations de copyright

© 2024. The Author(s), under exclusive licence to Springer Nature B.V.

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Auteurs

Farzaneh Motallebi (F)

Student Research Committee, Golestan University of Medical Sciences, Gorgan, Iran.

Zainab M Al Sudani (ZM)

Student Research Committee, Golestan University of Medical Sciences, Gorgan, Iran.

Fatemeh Vaghefi (F)

Student Research Committee, Golestan University of Medical Sciences, Gorgan, Iran.

Teymoor Khosravi (T)

Student Research Committee, Golestan University of Medical Sciences, Gorgan, Iran.

Arian Rahimzadeh (A)

Student Research Committee, Golestan University of Medical Sciences, Gorgan, Iran.

Ali Kowsari (A)

Pathology and Genetic Laboratory, Beski Hospital, Gonbad-e-Kavus, Golestan, Iran.

Morteza Oladnabi (M)

Gorgan Congenital Malformations Research Center, Golestan University of Medical Sciences, Gorgan, Iran. oladnabidozin@yahoo.com.
Ischemic Disorders Research Center, Golestan University of Medical Sciences, Gorgan, Iran. oladnabidozin@yahoo.com.
Department of Medical Genetics, School of Advanced Technologies in Medicine, Golestan University of Medical Sciences, Gorgan, Iran. oladnabidozin@yahoo.com.

Classifications MeSH