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Is a rare CXCL8 gene variant a new possible cause or course factor of inflammatory bowel disease?

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dc.abstract.enIntroduction: The pathogenesis of inflammatory bowel diseases (IBD) involves genetic, environmental, immunological, and microbial factors; however, it remains unclear. Pro-inflammatory interleukin 8 (IL-8), encoded by the CXCL8 gene, assumes a crucial chemotactic role in leukocyte migration. Methods: This study aimed to investigate whether an association exists between IBD and two CXCL8 variants, namely, c.-251A>T (rs4073) and c.91G>T (rs188378669), and IL-8 concentration. We analyzed the distribution of both variants among 353 Polish IBD patients and 200 population subjects using pyrosequencing, competitive allele-specific PCR and Sanger sequencing. Results: The c.91T stop-gained allele was significantly more frequent in IBD patients (2.12%) than in controls (0.25%) (p = 0.0121), while the c.-251T allele frequencies were similar (54% vs. 51.5%, p = 0.4955). Serum IL-8 concentrations, measured using ELISA, were higher in IBD patients with the c.91 GG genotype compared to healthy controls (mean, 70.02 vs. 51.5 pg/ml, p<0.01) and patients with c.91 GT (mean, 61.73 pg/ml). Moreover, clinical data indicated that carriers of the c.91T variant need more often corticosteroids and surgical treatment of the disease than GG homozygous IBD patients. Conclusion: This suggest that the CXCL8 c.91T allele may influence IBD manifestation and the course of the disorders in Polish patients, potentially serving as a novel target for future studies and therapeutic approaches
dc.affiliationWydział Rolnictwa, Ogrodnictwa i Biotechnologii
dc.affiliation.instituteKatedra Biochemii i Biotechnologii
dc.contributor.authorGabryel, Marcin
dc.contributor.authorZakerska-Banaszak, Oliwia
dc.contributor.authorLadziak, Karolina
dc.contributor.authorHubert, Katarzyna Anna
dc.contributor.authorBaturo, Alina
dc.contributor.authorSuszyńska-Zajczyk, Joanna
dc.contributor.authorHryhorowicz, Magdalena Julita
dc.contributor.authorDobrowolska, Agnieszka
dc.contributor.authorSkrzypczak-Zielinska, Marzena
dc.date.access2025-06-11
dc.date.accessioned2025-06-11T10:14:54Z
dc.date.available2025-06-11T10:14:54Z
dc.date.copyright2025-03-19
dc.date.issued2025
dc.description.abstract<jats:sec><jats:title>Introduction</jats:title><jats:p>The pathogenesis of inflammatory bowel diseases (IBD) involves genetic, environmental, immunological, and microbial factors; however, it remains unclear. Pro-inflammatory interleukin 8 (IL-8), encoded by the <jats:italic>CXCL8</jats:italic> gene, assumes a crucial chemotactic role in leukocyte migration.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>This study aimed to investigate whether an association exists between IBD and two <jats:italic>CXCL8</jats:italic> variants, namely, c.-251A&amp;gt;T (rs4073) and c.91G&amp;gt;T (rs188378669), and IL-8 concentration. We analyzed the distribution of both variants among 353 Polish IBD patients and 200 population subjects using pyrosequencing, competitive allele-specific PCR and Sanger sequencing.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>The c.91T stop-gained allele was significantly more frequent in IBD patients (2.12%) than in controls (0.25%) (<jats:italic>p</jats:italic> = 0.0121), while the c.-251T allele frequencies were similar (54% vs. 51.5%, <jats:italic>p</jats:italic> = 0.4955). Serum IL-8 concentrations, measured using ELISA, were higher in IBD patients with the c.91 GG genotype compared to healthy controls (mean, 70.02 vs. 51.5 pg/ml, <jats:italic>p</jats:italic>&amp;lt;0.01) and patients with c.91 GT (mean, 61.73 pg/ml). Moreover, clinical data indicated that carriers of the c.91T variant need more often corticosteroids and surgical treatment of the disease than GG homozygous IBD patients.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>This suggest that the <jats:italic>CXCL8</jats:italic> c.91T allele may influence IBD manifestation and the course of the disorders in Polish patients, potentially serving as a novel target for future studies and therapeutic approaches.</jats:p></jats:sec>
dc.description.accesstimeat_publication
dc.description.bibliographyil., bibliogr.
dc.description.financeother
dc.description.financecost2500,00
dc.description.if5,7
dc.description.points140
dc.description.versionfinal_published
dc.description.volume16
dc.identifier.doi10.3389/fimmu.2025.1562618
dc.identifier.issn1664-3224
dc.identifier.urihttps://sciencerep.up.poznan.pl/handle/item/2828
dc.identifier.weblinkhttps://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2025.1562618/full
dc.languageen
dc.relation.ispartofFrontiers in Immunology
dc.relation.pagesart. 1562618
dc.rightsCC-BY
dc.sciencecloudnosend
dc.share.typeOPEN_JOURNAL
dc.subject.enCXCL8 gene
dc.subject.eninflammatory bowel disease (IBD)
dc.subject.eninflammation
dc.subject.eninterleukin 8
dc.subject.engenetic variants
dc.subject.enCrohns disease
dc.subject.encolitis ulcerosa
dc.titleIs a rare CXCL8 gene variant a new possible cause or course factor of inflammatory bowel disease?
dc.typeJournalArticle
dspace.entity.typePublication
oaire.citation.volume16