2019
DOI: 10.1080/20905068.2019.1592938
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Interleukin-1 single nucleotide polymorphisms as risk factors for susceptibility of inflammatory bowel disease: an Iraqi Arab population-based study

Abstract: Objectives: It is aimed to determine the association between four single-nucleotide polymorphisms (SNPs) of IL1 genes (rs1800587: IL1A −889 C/T, rs16944: IL1B −511 T/C, rs2234650: IL1R1 pst1 1970 T/C and rs315952: IL1RA mspa1 11100 T/C) and the two types of IBD (UC and CD) in samples of Iraqi Arab patients. Materials and Methods: Hundred Iraqi patients (66 UC and 34 CD) were genotyped for these SNPs by polymerase chain reaction-specific sequence primer (PCR-SSP) assay. Results: A significant increased frequenc… Show more

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Cited by 4 publications
(2 citation statements)
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“…Indeed, IL-1β promotes Th17 responses, suggesting synergistic interactions with IL-23 signals that sustain innate and adaptive inflammatory responses in the gut; moreover, the IL-1β regulation of Th17 can be induced by a MyD88-dependent microbial signal [74]. In addition, in this case, particular IL1B polymorphisms were significantly associated with the risk of IBD [75,76], conferring to the IL-1β drug silencing a potential therapy role, especially for patients caring these variants or for those with deep ulceration and who do not respond to several different current therapeutics [77]. In this study, an increase in IL1B gene expression in Caco-2 cells and IL-1β release for both Caco-2 and THP-1 cells was observed after pro-inflammatory stimuli induction.…”
Section: Discussionmentioning
confidence: 94%
“…Indeed, IL-1β promotes Th17 responses, suggesting synergistic interactions with IL-23 signals that sustain innate and adaptive inflammatory responses in the gut; moreover, the IL-1β regulation of Th17 can be induced by a MyD88-dependent microbial signal [74]. In addition, in this case, particular IL1B polymorphisms were significantly associated with the risk of IBD [75,76], conferring to the IL-1β drug silencing a potential therapy role, especially for patients caring these variants or for those with deep ulceration and who do not respond to several different current therapeutics [77]. In this study, an increase in IL1B gene expression in Caco-2 cells and IL-1β release for both Caco-2 and THP-1 cells was observed after pro-inflammatory stimuli induction.…”
Section: Discussionmentioning
confidence: 94%
“…In UC, the stimulation of white blood cells arises after bacterial imbalance and infection in the gut, along with an impaired mucosal barrier. Even if the infection subsides, the response of the immune system continues, leading to chronicity (3,4). One of the scoring systems that clinicians use to estimate the clinical severity of UC is the Simple Clinical Colitis Activity Index (SCCAI), which offers an easy way of detecting possible relapse and decreases the need for invasive and uncomfortable examinations or laboratory tests (5,6).…”
Section: Introduction Introductionmentioning
confidence: 99%