CCR5Δ32 Polymorphism and Inflammatory Bowel Disease: A Case–Control and Genotype–Phenotype Study in a Polish Population
- 1Department of Clinical Pharmacology, Wroclaw Medical University, Borowska 211A, 50-556 Wroclaw, Poland
- 2Department of Gastroenterology and Internal Medicine, University Clinical Center, Medical University of Warsaw, Banacha 1A, 02-097 Warsaw, Poland
- 3Department of Gastroenterology, Hepatology and Internal Medicine, Wroclaw Medical University, Borowska 213, 50-556 Wroclaw, Poland
Abstract
C-C chemokine receptor 5 (CCR5) contributes to leukocyte trafficking and intestinal inflammation, whereas the functional CCR5Δ32 deletion markedly impairs receptor expression. Its role in inflammatory bowel disease (IBD) susceptibility remains uncertain. We evaluated CCR5Δ32 in 274 patients with IBD, including 141 with Crohn’s disease (CD) and 133 with ulcerative colitis (UC), and 100 controls using polymerase chain reaction genotyping; phenotype-related associations were explored in a clinically characterized subgroup. Overall CCR5 genotype distributions did not differ between patients with IBD and controls (p = 0.11). In the dominant model, CCR5Δ32 carriage was not associated with IBD overall (OR = 0.67, 95% CI 0.39–1.14; nominal p = 0.139; Holm-adjusted p = 0.319), CD, or UC. The CCR5Δ32 allele was nominally less frequent in UC than in controls (9.0% vs. 15.0%; OR = 0.56, 95% CI 0.317–0.995; p = 0.046), but this exploratory allele-level signal was not supported by the dominant model. CCR5Δ32 carriage was more frequent in men than women with IBD (OR = 2.07, 95% CI 1.06–4.03; p = 0.031), although the carrier-by-sex interaction for IBD susceptibility was not significant (p = 0.441). Direct within-disease phenotype comparisons were also non-significant; the strongest signal was lower carriage in corticosteroid-exposed versus unexposed UC (OR = 0.26, 95% CI 0.05–1.28; p = 0.065). CCR5Δ32 does not appear to be a major IBD susceptibility variant, but the UC-, sex-, and phenotype-related observations warrant independent replication.
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BibTeX
@article{petryszyn2026ccr5δ32,
title = {{CCR5Δ32 Polymorphism and Inflammatory Bowel Disease: A Case–Control and Genotype–Phenotype Study in a Polish Population}},
author = {Pawel Petryszyn and Klaudia Koj and Robert Dudkowiak and Agnieszka Gruca and Elzbieta Poniewierka and Krystyna Głowacka},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = sep,
doi = {10.3390/ijms27188297},
url = {https://www.mdpi.com/1422-0067/27/18/8297},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - CCR5Δ32 Polymorphism and Inflammatory Bowel Disease: A Case–Control and Genotype–Phenotype Study in a Polish Population
AU - Pawel Petryszyn
AU - Klaudia Koj
AU - Robert Dudkowiak
AU - Agnieszka Gruca
AU - Elzbieta Poniewierka
AU - Krystyna Głowacka
PY - 2026
DA - 2026/09/17
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27188297
UR - https://www.mdpi.com/1422-0067/27/18/8297
AB - C-C chemokine receptor 5 (CCR5) contributes to leukocyte trafficking and intestinal inflammation, whereas the functional CCR5Δ32 deletion markedly impairs receptor expression. Its role in inflammatory bowel disease (IBD) susceptibility remains uncertain. We evaluated CCR5Δ32 in 274 patients with IBD, including 141 with Crohn’s disease (CD) and 133 with ulcerative colitis (UC), and 100 controls using polymerase chain reaction genotyping; phenotype-related associations were explored in a clinically characterized subgroup. Overall CCR5 genotype distributions did not differ between patients with IBD and controls (p = 0.11). In the dominant model, CCR5Δ32 carriage was not associated with IBD overall (OR = 0.67, 95% CI 0.39–1.14; nominal p = 0.139; Holm-adjusted p = 0.319), CD, or UC. The CCR5Δ32 allele was nominally less frequent in UC than in controls (9.0% vs. 15.0%; OR = 0.56, 95% CI 0.317–0.995; p = 0.046), but this exploratory allele-level signal was not supported by the dominant model. CCR5Δ32 carriage was more frequent in men than women with IBD (OR = 2.07, 95% CI 1.06–4.03; p = 0.031), although the carrier-by-sex interaction for IBD susceptibility was not significant (p = 0.441). Direct within-disease phenotype comparisons were also non-significant; the strongest signal was lower carriage in corticosteroid-exposed versus unexposed UC (OR = 0.26, 95% CI 0.05–1.28; p = 0.065). CCR5Δ32 does not appear to be a major IBD susceptibility variant, but the UC-, sex-, and phenotype-related observations warrant independent replication.
SN - 1422-0067
ER -