BACKGROUND AND PURPOSE: Necrotizing enterocolitis (NEC) is a leading cause of morbidity and mortality among premature infants. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that has been implicated in the pathophysiology of inflammatory bowel diseases. The MIF promoter contains a functionally relevant single nucleotide polymorphism (SNP) G→C at position -173, with the MIF -173*C allele being associated with higher MIF expression in vitro and with higher MIF levels in vivo. The aim of this study was to investigate whether the G/C polymorphism at -173 of the MIF promoter is associated with the development of NEC. METHODS: In this retrospective cohort study, 107 preterm infants (GA ≤ 32 weeks), of whom 41 had NEC (NEC Stage I n = 20, Stage II n = 3, Stage III n = 18) and 66 were not affected, were genotyped for the MIF -173 SNP. MIF genotyping was carried out by PCR and DHPLC. RESULTS: We did not find significant differences in the prevalence of the -173G/C polymorphism and in the distribution of the -173 MIF genotype in infants with NEC compared to controls. Moreover, we did not observe an association between the polymorphism and mortality. CONCLUSIONS: The polymorphism -173G/C of the MIF promoter does not appear to be of major importance in the pathophysiology of NEC in preterm infants.
BACKGROUND AND PURPOSE:Necrotizing enterocolitis (NEC) is a leading cause of morbidity and mortality among premature infants. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that has been implicated in the pathophysiology of inflammatory bowel diseases. The MIF promoter contains a functionally relevant single nucleotide polymorphism (SNP) G→C at position -173, with the MIF -173*C allele being associated with higher MIF expression in vitro and with higher MIF levels in vivo. The aim of this study was to investigate whether the G/C polymorphism at -173 of the MIF promoter is associated with the development of NEC. METHODS: In this retrospective cohort study, 107 preterm infants (GA ≤ 32 weeks), of whom 41 had NEC (NEC Stage I n = 20, Stage II n = 3, Stage III n = 18) and 66 were not affected, were genotyped for the MIF -173 SNP. MIF genotyping was carried out by PCR and DHPLC. RESULTS: We did not find significant differences in the prevalence of the -173G/C polymorphism and in the distribution of the -173 MIF genotype in infants with NEC compared to controls. Moreover, we did not observe an association between the polymorphism and mortality. CONCLUSIONS: The polymorphism -173G/C of the MIF promoter does not appear to be of major importance in the pathophysiology of NEC in preterm infants.
Authors: Tamas Jilling; Namasivayam Ambalavanan; C Michael Cotten; Colin A Martin; Akhil Maheshwari; Kurt Schibler; Joshua Levy; Grier P Page Journal: Pediatr Res Date: 2018-05-16 Impact factor: 3.756