Association of interleukin-10 gene haplotypes with Pseudomonas aeruginosa airway colonization in cystic fibrosis

Abstract

We genotyped three polymorphisms of the promoter region of the interleukin-10 (IL-10) gene in 220 CF patients from the CF Center of Bari, and tested for an association between genetic variants of the cytokine and chronic airway colonization with Pseudomonas aeruginosa. We found that carriers of the high-IL-10-producing-GCC haplotype had significantly higher risk of chronic pulmonary infection with the pathogen.

Inverse correlation between HPSE gene single nucleotide polymorphisms and heparanase expression: possibility of multiple levels of heparanase regulation

“…Specifically, the GCC haplotype of IL-10 gene SNPs is associated with a higher production of IL-10 by peripheral blood mononuclear cells, while the ATA haplotype is associated with low production [55]. Genotypes of IL-10 low producers correlate with the control of inflammatory responses and low susceptibility to inflammation and infection [56,57]. Thus, carriers of the high IL-10-producing GCC haplotype exhibited a significantly higher risk of infection [56,57].…”

“…Genotypes of IL-10 low producers correlate with the control of inflammatory responses and low susceptibility to inflammation and infection [56,57]. Thus, carriers of the high IL-10-producing GCC haplotype exhibited a significantly higher risk of infection [56,57]. However, as for cardiovascular diseases, the low IL-10 producer -1082AA genotype was associated with elevated levels of serum C reactive protein (CRP), predictive for a higher cardiovascular morbidity in patients undergoing dialysis.…”

Pathogen and autoantigen homologous regions within the cystic fibrosis transmembrane conductance regulator (CFTR) protein suggest an autoimmune treatable component of cystic fibrosis

“…Many genes that modify the progression or the severity of cystic fibrosis are related to immune function. These include inflammation-related genes [interleukins IL1B, IL8 and IL10, transforming growth factor-b1, tumour necrosis factor (TNF)-a and its receptor TNFR], antioxidant-related genes (glutathione-S-transferase), prostaglandin-endoper-oxide synthase genes (COX1 and COX2) as well as CD95, Toll receptor TLR9, T cell receptor-b and HLA antigens (McMillan et al, 1989;Merlo & Boyle, 2003;Hillian et al, 2008;Tesse et al, 2008;Levy et al, 2009;Czerska et al, 2010;Stanke et al, 2010). Several major histocompatibility complex molecules, including HLA-DR2, HLA-DQB1 Ã 0201, HLA-DRB1 Ã 0301, and DR7/DQA Ã 0201 and HLA-B-18, have all been associated with cystic fibrosis symptomatology or pathogen colonization (Kaiser et al, 1977;Libby et al, 1983;Aron et al, 1999;Laki et al, 2006).…”

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“…А Таблица 3 -Показатели иммунного статуса детей с муковисцидозом в зависимости от мутаций генов интерлейкина-4 и интерлейкина-10 Примечание: различия между группами: р 1 -основной и сравнения; р 2 -основной и контрольной; р 3 -сравнения и контрольной. исследование R. Tesse (2008), наоборот, доказывает сильную достоверную связь между мутацией гена ИЛ-10 и частотой инфицирования синегнойной палочкой [17]. Наше исследование также не выявило достоверных связей распространения данного патогена в группе с наличием мутантных аллелей генов цитокинов ИЛ-4 и ИЛ-10, но доказаны более ранние сроки инфицирования S. aureus и C. albicans.…”