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Association Between Gene Polymorphisms of IRAK-M and the Susceptibility of Sepsis

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Abstract

The aim of this study was to explore the association between the single-nucleotide polymorphisms of interleukin-1 receptor-associated kinase-M (IRAK-M) gene and the susceptibility of sepsis. The allele frequency and genotype distribution of IRAK-M gene polymorphisms were assessed in 118 controls and 82 sepsis patients by semiquantitative polymerase chain reaction and restriction fragment length polymorphism (RFLP) analysis. The plasma levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were detected by enzyme-linked immunosorbent assay. Associations between IRAK-M polymorphisms and the susceptibility of sepsis were analyzed by Cox regression. Data were analyzed by the χ 2 test and the Student’s t test, whenever appropriate. Statistical calculations were performed by using statistical package SPSS version 18.0. The genotype distribution of IRAK-M+22148 polymorphism significantly differed between the sepsis and control groups (P < 0.0001). The frequency of the G allele was remarkably more common in the sepsis group than that of the control group (P < 0.0001). However, the frequency of the A allele was significantly less common in the sepsis group than that of control group (P < 0.0001). Moreover, the plasma levels (in picograms per milliliter) of TNF-α and IL-6 in patients with G/G genotype were greatly higher than those with A/A genotype after lipopolysaccharide stimulation (P < 0.05). The genetic polymorphism of IRAK-M+22148 G>A is associated with the susceptibility of sepsis. The G/G genotype of IRAK-M increases the risk of developing sepsis, and the A/A genotype may play a protective role in the process of developing sepsis.

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Acknowledgments

This project was granted financial support from the National Natural Science Foundation of China (grant 30471696).

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Correspondence to Kun He.

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Dong, Gh., Gong, Jp., Li, Jz. et al. Association Between Gene Polymorphisms of IRAK-M and the Susceptibility of Sepsis. Inflammation 36, 1087–1093 (2013). https://doi.org/10.1007/s10753-013-9641-z

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