Abstract
The present study was performed to investigate the association between interleukin-17 (IL-17) and nuclear factor κB (NF-κB) gene polymorphisms and the risk and prognosis of acute respiratory distress syndrome (ARDS) in a Chinese population. A total of 210 Chinese patients with ARDS were selected as the study group, 210 individuals who were identified as at-risk patients but did not meet criteria for ARDS were recruited as the control group. Three single nucleotide polymorphisms (SNPs) of IL-17, including rs763780 (A>G), rs2275913 (G>A), rs8193036 (C>T) and NF-κB1 gene rs3774934 (G>A) loci were examined by Sanger sequencing technique in the peripheral blood of all subjects. Patients were followed for 30-day survival. The IL-17 rs763780 and NF-κB1 rs3774934 SNPs had no impact on ARDS risk and prognosis of ARDS (P>0.05). Compared with individuals carrying the wild-type GG genotype of rs2275913 at IL-17, the AA-homozygous and GA- heterozygous individuals were protected from the development of ARDS. Consistently, a decreased 30-day mortality risk was found among A-allele carriers of rs2275913 at IL-17 (p<0.05). For IL-17 rs8193036 SNP, the homozygote TT genotype and heterozygote CT genotypes were associated with increased ARDS susceptibility and 30-day mortality risk (P<0.05). Besides, decreased IL-17 levels were found in A-allele carriers of IL-17 rs2275913, whereas individuals carrying T-allele of IL-17 rs8193036 were found to have significantly increased levels of IL-17 (P<0.05). Our results suggested that two functional polymorphisms of IL-17, rs2275913 and rs8193036 were associated with ARDS risk and prognosis, indicating that the two genetic variants might act as possible markers for the prediction of ARDS risk and development.
Highlights
Acute respiratory distress syndrome (ARDS) is a devastating clinical syndrome which is most commonly a manifestation of sepsis-induced organ dysfunction, characterized by disruption of endothelial barrier integrity and diffuse lung damage [1]
From May 2014 to October 2017, a total of 210 consecutive patients with ARDS admitted to our intensive care unit (ICU) at the Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University were enrolled in the present study as the case group, 210 controls were enrolled from individuals who were identified as at-risk patients who did not meet criteria for ARDS during the ICU stay and had no prior history of ARDS
The control group enrolled 210 individuals who were identified as at-risk patients but did not meet criteria for ARDS, 103 males and 107 females with the mean age of 57.4 +− 9.1 years
Summary
Acute respiratory distress syndrome (ARDS) is a devastating clinical syndrome which is most commonly a manifestation of sepsis-induced organ dysfunction, characterized by disruption of endothelial barrier integrity and diffuse lung damage [1]. This can result in increased vascular permeability of alveolar-capillary membrane, acute onset of pulmonary edema, along with bilateral pulmonary infiltrates and decreased lung compliance that patients with ARDS need supportive care in the intensive care unit (ICU) to maintain oxygenation and prevent adverse outcomes [2,3]. Interleukin-17 (IL-17) is a proinflammatory cytokine produced by the memory CD4 + T cells
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