Funisitis is associated with increased interleukin-10 gene expression in cord blood mononuclear cells in preterm infants ≤32 weeks of gestation

Objectives: A systemic inflammatory response after intrauterine funisitis is assumed to be an important priming factor for acute and chronic pulmonary morbidity and neurological impairment in premature infants. Fetal lymphocytes and monocytes modulate the primary immune response. Genetic regulation of the cytokine-mediated process is partially known. The objective of our study was to examine the pro-inflammatory and anti-inflammatory responses in umbilical cord blood mononuclear cells (CBMC) of preterm infants on the transcriptional level. Study design: Fifteen preterm infants with a gestational age <= 32 weeks were enrolled in this prospective study. Funisitis was diagnosed in five of the 15 by histological examination. Gene expression of pro-inflammatory cytokines (TNF-alpha., IL-8, IL-1 beta and IL-17) and anti-inflammatory cytokines (IL-10 and TGF-beta 1) was examined in CBMC by real time reverse transcription polymerase chain reaction. Results: Gene expression of IL-10 was significantly higher in the funisitis group compared to unexposed controls (p < 0.008). Expression of TGF-beta 1 TNF-a, IL-8 and IL-1 beta did not differ significantly between the funisitis and control group. IL-17 was detectable in only two samples. Conclusions: Funisitis is associated with increased IL-10 gene expression in CBMC of preterm infants with a gestational age <= 32 weeks. This might contribute to modulation of postnatal immunoreactions and immunoregulation in these individuals. (C) 2010 Elsevier Ireland Ltd. All rights reserved.