The macrophage migration inhibitory factor −173G/C polymorphism is not significantly associated with necrotizing enterocolitis in preterm infants
| Autor: | Giusi Prencipe, Rita Inglese, Cinzia Auriti, Fabrizio De Benedetti, Andrea Dotta, G. Gallusi |
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| Rok vydání: | 2013 |
| Předmět: |
medicine.medical_treatment
chemical and pharmacologic phenomena Single-nucleotide polymorphism Infant Premature Diseases Cohort Studies Enterocolitis Necrotizing Genotype otorhinolaryngologic diseases medicine Humans SNP Macrophage Migration-Inhibitory Factors Genotyping Retrospective Studies Polymorphism Genetic business.industry Cytokines Innate immunity MIF NEC Infant Newborn Infant Premature Intramolecular Oxidoreductases Surgery Pediatrics Perinatology and Child Health General Medicine respiratory system medicine.disease biological factors digestive system diseases Pathophysiology Cytokine Immunology Necrotizing enterocolitis Macrophage migration inhibitory factor business |
| Zdroj: | Journal of Pediatric Surgery. 48:1499-1502 |
| ISSN: | 0022-3468 |
| DOI: | 10.1016/j.jpedsurg.2013.01.004 |
| Popis: | 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≤32weeks), 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. |
| Databáze: | OpenAIRE |
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