In:
Mediators of Inflammation, Hindawi Limited, Vol. 2018 ( 2018), p. 1-8
Abstract:
DEFA1/DEFA3, genes encoding human neutrophil peptides (HNP) 1–3, display wide-ranging copy number variations (CNVs) and is functionally associated with innate immunity and infections. To identify potential associations between DEFA1/DEFA3 CNV and hospital-acquired infections (HAIs), we enrolled 106 patients with HAIs and 109 controls in the intensive care unit (ICU) and examined their DEFA1/DEFA3 CNVs. DEFA1/DEFA3 copy number ranged from 2 to 16 per diploid genome in all 215 critically ill patients, with a median of 7 copies. In HAIs, DEFA1/DEFA3 CNV varied from 2 to 12 with a median of 6, which was significantly lower than that in controls (2 to 16 with a median of 8, p = 0.017 ). Patients with lower DEFA1/DEFA3 copy number (CNV 〈 7) were far more common in HAIs than in controls (52.8% in HAIs versus 35.8% in controls; p = 0.014 ; OR, 2.010; 95% CI, 1.164–3.472). The area under the receiver operating characteristic (AUROC) of DEFA1/DEFA3 CNV combined with clinical characteristics to predict the incidence of HAIs was 0.763 (95% CI 0.700–0.827), showing strong predictive ability. Therefore, lower DEFA1/DEFA3 copy number contributes to higher susceptibility to HAIs in critically ill patients, and DEFA1/DEFA3 CNV is a significant hereditary factor for predicting HAIs.
Type of Medium:
Online Resource
ISSN:
0962-9351
,
1466-1861
DOI:
10.1155/2018/2152650
Language:
English
Publisher:
Hindawi Limited
Publication Date:
2018
detail.hit.zdb_id:
2008065-7
