Dataset Information

Association of Rs7217186 Polymorphism of Arachidonic Acid 15-Lipoxygenase (ALOX15) Gene with Susceptibility to Allergic Rhinitis.

ABSTRACT:

Background

Allergic rhinitis (AR) is an inflammatory disorder of the nasal mucosa, caused by exposure to environmental allergens. It is known that 15-lipoxygenase (15-LOX) is involved in the biosynthetic pathways of anti-inflammatory lipid mediators, including resolvins and protectins.

Methods

In this study, which was performed on 130 AR patients and 130 healthy controls, we aimed to investigate the association of susceptibility to AR with two selected single-nucleotide polymorphisms (SNPs), that is, rs2619112:A>G and rs7217186:C>T, in the intron regions of arachidonic acid 15-LOX (ALOX15) gene, using SNPinfo and Regulome DB tools.

Results

The results showed that the CT genotype of rs7217186: C>T was significantly associated with the increased risk of AR compared to the CC genotype (P= 0.037, OR=1.943, CI: 1.038-0.638). However, there was no strong evidence of the association of rs2619112: A>G with susceptibility to AR (P> 0.05).

Conclusions

The present results indicated that rs7217186 polymorphism of ALOX15 gene might be a potential biomarker for susceptibility to AR.

SUBMITTER: Eivazi A

PROVIDER: S-EPMC10838593 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature

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Publications

Association of Rs7217186 Polymorphism of Arachidonic Acid 15-Lipoxygenase (ALOX15) Gene with Susceptibility to Allergic Rhinitis.

Eivazi Atefeh A Akbari Bahman B Falahi Sara S Gorgin Karaji Ali A Rezaiemanesh Alireza A Mortazavi Seyed Hamid Reza SHR Daneshfar Niloofar N Salari Farhad F

Reports of biochemistry & molecular biology 20230701 2

<h4>Background</h4>Allergic rhinitis (AR) is an inflammatory disorder of the nasal mucosa, caused by exposure to environmental allergens. It is known that 15-lipoxygenase (15-LOX) is involved in the biosynthetic pathways of anti-inflammatory lipid mediators, including resolvins and protectins.<h4>Methods</h4>In this study, which was performed on 130 AR patients and 130 healthy controls, we aimed to investigate the association of susceptibility to AR with two selected single-nucleotide polymorphi ...[more]

PMID: 38317810

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Project description:Macrophages acquire anti-inflammatory and proresolving functions to facilitate resolution of inflammation and promote tissue repair. While alternatively activated macrophages (AAMs), also referred to as M2 macrophages, polarized by type 2 (Th2) cytokines IL-4 or IL-13 contribute to the suppression of inflammatory responses and play a pivotal role in wound healing, contemporaneous exposure to apoptotic cells (ACs) potentiates the expression of anti-inflammatory and tissue repair genes. Given that liver X receptors (LXRs), which coordinate sterol metabolism and immune cell function, play an essential role in the clearance of ACs, we investigated whether LXR activation following engulfment of ACs selectively potentiates the expression of Th2 cytokine-dependent genes in primary human AAMs. We show that AC uptake simultaneously upregulates LXR-dependent, but suppresses SREBP-2-dependent gene expression in macrophages, which are both prevented by inhibiting Niemann-Pick C1 (NPC1)-mediated sterol transport from lysosomes. Concurrently, macrophages accumulate sterol biosynthetic intermediates desmosterol, lathosterol, lanosterol, and dihydrolanosterol but not cholesterol-derived oxysterols. Using global transcriptome analysis, we identify anti-inflammatory and proresolving genes including interleukin-1 receptor antagonist (IL1RN) and arachidonate 15-lipoxygenase (ALOX15) whose expression are selectively potentiated in macrophages upon concomitant exposure to ACs or LXR agonist T0901317 (T09) and Th2 cytokines. We show priming macrophages via LXR activation enhances the cellular capacity to synthesize inflammation-suppressing specialized proresolving mediator (SPM) precursors 15-HETE and 17-HDHA as well as resolvin D5. Silencing LXRα and LXRβ in macrophages attenuates the potentiation of ALOX15 expression by concomitant stimulation of ACs or T09 and IL-13. Collectively, we identify a previously unrecognized mechanism of regulation whereby LXR integrates AC uptake to selectively shape Th2-dependent gene expression in AAMs.

Dataset Information

Association of Rs7217186 Polymorphism of Arachidonic Acid 15-Lipoxygenase (ALOX15) Gene with Susceptibility to Allergic Rhinitis.

Background

Methods

Results

Conclusions

Publications

Association of Rs7217186 Polymorphism of Arachidonic Acid 15-Lipoxygenase (ALOX15) Gene with Susceptibility to Allergic Rhinitis.

Similar Datasets

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