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Association of IL13R alpha 1 +1398A/G polymorphism in a North Indian population with asthma: A case-control study.

Sinha S, Singh J, Jindal SK, Birbian N - Allergy Rhinol (Providence) (2015)

Bottom Line: One of the polymorphic receptor of IL13 is IL13Rα1, which after binding to IL13, initiates signal transduction that results in mucin secretion, airway hyperreactivity, fibrosis, and chitinase up-regulation, which increases asthma risk.Furthermore, the phenotypic characteristics also reveal a significant association with the disease (p < 0.05).This is the first study conducted in India and +1398A/G polymorphism in noncoding region of IL13Rα1 confer risk toward asthma in the studied population.

View Article: PubMed Central - PubMed

Affiliation: Department of Biotechnology, Panjab University, Chandigarh, India.

ABSTRACT

Background: Interleukin 13 (IL13) is directly involved in the secretion of total serum immunoglobulin E (IgE), which plays a major role in the asthma pathogenesis.

Objective: One of the polymorphic receptor of IL13 is IL13Rα1, which after binding to IL13, initiates signal transduction that results in mucin secretion, airway hyperreactivity, fibrosis, and chitinase up-regulation, which increases asthma risk.

Methods: In the present study, the role of IL13Rα1 +1398A/G gene polymorphisms in asthma was detected with a total of 964 individuals, including 483 healthy controls and 481 asthma patients from a North Indian population using polymerase chain reaction-restriction fragment length polymorphism method.

Results: Statistical analysis revealed that the mutant allele (G) is predominant in asthma patients (42.7%) than the controls (38.2%), which shows an increased risk toward asthma with odds ratio = 1.21, 95% confidence interval (1.00-1.45), χ(2) = 4.10 and p = 0.043. Furthermore, the phenotypic characteristics also reveal a significant association with the disease (p < 0.05).

Conclusions: This is the first study conducted in India and +1398A/G polymorphism in noncoding region of IL13Rα1 confer risk toward asthma in the studied population.

No MeSH data available.


Related in: MedlinePlus

Restriction digestion (MseI) products of IL13Rα1 +1398A//G polymorphism on 3% Agarose gel. Lane 1: 20 bp ladder. Lane 2: heterozygous AG genotype (130, 85, and 45 bp). Lane 3: homozygous mutant GG genotype (130 bp). Lane 4: homozygous wild AA genotype (85 and 45 bp).
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Figure 1: Restriction digestion (MseI) products of IL13Rα1 +1398A//G polymorphism on 3% Agarose gel. Lane 1: 20 bp ladder. Lane 2: heterozygous AG genotype (130, 85, and 45 bp). Lane 3: homozygous mutant GG genotype (130 bp). Lane 4: homozygous wild AA genotype (85 and 45 bp).

Mentions: The amplification of the IL13Rα1 +1398A/G polymorphism was done using polymerase chain reaction-restriction fragment length polymorphism method17 using MseI (New England BioLabs, Hitchin, United Kingdom) (Fig. 1). The primer sequences were: Forward 5′-TCAGTGATGGAGATAATTTA-3′ and Reverse 5′-TGAGCTGCCTGTTTATAAAT-3′.


Association of IL13R alpha 1 +1398A/G polymorphism in a North Indian population with asthma: A case-control study.

Sinha S, Singh J, Jindal SK, Birbian N - Allergy Rhinol (Providence) (2015)

Restriction digestion (MseI) products of IL13Rα1 +1398A//G polymorphism on 3% Agarose gel. Lane 1: 20 bp ladder. Lane 2: heterozygous AG genotype (130, 85, and 45 bp). Lane 3: homozygous mutant GG genotype (130 bp). Lane 4: homozygous wild AA genotype (85 and 45 bp).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4541631&req=5

Figure 1: Restriction digestion (MseI) products of IL13Rα1 +1398A//G polymorphism on 3% Agarose gel. Lane 1: 20 bp ladder. Lane 2: heterozygous AG genotype (130, 85, and 45 bp). Lane 3: homozygous mutant GG genotype (130 bp). Lane 4: homozygous wild AA genotype (85 and 45 bp).
Mentions: The amplification of the IL13Rα1 +1398A/G polymorphism was done using polymerase chain reaction-restriction fragment length polymorphism method17 using MseI (New England BioLabs, Hitchin, United Kingdom) (Fig. 1). The primer sequences were: Forward 5′-TCAGTGATGGAGATAATTTA-3′ and Reverse 5′-TGAGCTGCCTGTTTATAAAT-3′.

Bottom Line: One of the polymorphic receptor of IL13 is IL13Rα1, which after binding to IL13, initiates signal transduction that results in mucin secretion, airway hyperreactivity, fibrosis, and chitinase up-regulation, which increases asthma risk.Furthermore, the phenotypic characteristics also reveal a significant association with the disease (p < 0.05).This is the first study conducted in India and +1398A/G polymorphism in noncoding region of IL13Rα1 confer risk toward asthma in the studied population.

View Article: PubMed Central - PubMed

Affiliation: Department of Biotechnology, Panjab University, Chandigarh, India.

ABSTRACT

Background: Interleukin 13 (IL13) is directly involved in the secretion of total serum immunoglobulin E (IgE), which plays a major role in the asthma pathogenesis.

Objective: One of the polymorphic receptor of IL13 is IL13Rα1, which after binding to IL13, initiates signal transduction that results in mucin secretion, airway hyperreactivity, fibrosis, and chitinase up-regulation, which increases asthma risk.

Methods: In the present study, the role of IL13Rα1 +1398A/G gene polymorphisms in asthma was detected with a total of 964 individuals, including 483 healthy controls and 481 asthma patients from a North Indian population using polymerase chain reaction-restriction fragment length polymorphism method.

Results: Statistical analysis revealed that the mutant allele (G) is predominant in asthma patients (42.7%) than the controls (38.2%), which shows an increased risk toward asthma with odds ratio = 1.21, 95% confidence interval (1.00-1.45), χ(2) = 4.10 and p = 0.043. Furthermore, the phenotypic characteristics also reveal a significant association with the disease (p < 0.05).

Conclusions: This is the first study conducted in India and +1398A/G polymorphism in noncoding region of IL13Rα1 confer risk toward asthma in the studied population.

No MeSH data available.


Related in: MedlinePlus