Genetic variations in inflammation-related genes and their influence on the susceptibility of pediatric acute lung injury in a Chinese population

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Abstract

Acute lung injury (ALI) is a serious clinical syndrome that can cause respiratory failure and threaten the life of the patients. A biomarker that can predict the syndrome can contribute to a better clinical management of the patients. In adults, genetic polymorphisms in inflammatory-response genes have been shown to be a promising biomarker. However, the pathogenesis of ALI in adult is known to be different from that in children and no previous study has investigated the association between inflammatory gene polymorphisms and pediatric ALI (PALI) risk. In this work, we examined the association between 12 polymorphisms in six inflammatory-response genes (TNF, IL6, IL10, IL18, NFKB1 and NFKBIA) and risk of PALI. A total of 1075 children with ALI and 1382 non-ALI controls were recruited. The polymorphisms were genotyped employing RFLP method. The risk association was estimated via logistic regression analysis, with P < 0.004 being statistically significant after Bonferroni correction. A statistically significant association was observed for IL10 rs1800896 (heterozygous, P < 0.0001; homozygous variant, P < 0.0001; allele, P < 0.0001) and TNF rs1800629 (heterozygous, P < 0.0001; homozygous variant, P = 0.0012; allele, P < 0.0001) polymorphisms. On the other hand, no significant association was found for IL6 rs1800795, rs1800796 and rs1800797 polymorphisms, IL10 rs3021097 polymorphism, NFKB1 rs28362491 polymorphism, NFKBIA rs2233406 and rs696 polymorphisms, IL18 rs1946518 and rs187238 polymorphisms, and TNF rs1799964 polymorphism. In conclusion, IL10 rs1800896 and TNF rs1800629 may serve as a risk biomarker for pediatric ALI among Chinese.

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Zhao, X., He, J., Xie, G., Xu, S., Xie, J., Chen, Y., & Wu, H. (2019). Genetic variations in inflammation-related genes and their influence on the susceptibility of pediatric acute lung injury in a Chinese population. Gene, 687, 16–22. https://doi.org/10.1016/j.gene.2018.11.009

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