Objective: To investigate the hypothesis that preterm infants who are more susceptible to lung damage have decreased neutrophil apoptosis, and to explore its relation to interleukin 10 (IL10) concentration.
Design: Prospective cohort design.
Patients: One hundred tracheal fluid specimens from 50 week-1 ventilated infants were examined for IL10 (by enzyme linked immunosorbent assay) and neutrophil apoptosis (by light microscopy).
Results: Neutrophil apoptosis was absent or less than 0.22% (median 0%) in the 11 infants with chronic lung disease (CLD) (24–31 weeks gestation) during the first 4 days of life. This was significantly lower than that of the 20 preterm infants without CLD (27–31 weeks gestation; median 0.47%, range 0–1.25%) and 19 term infants (median 0.5%, range 0–2.25%). There was an increase in apoptosis in infants with CLD (median 0.44%, p = 0.046) during days 5–7. Few infants without CLD were intubated beyond 4 days. Median apoptosis on days 5–7 was 0.26% and 2.78% for non-CLD preterm and term infants, but differences were not significant. IL10 concentration in tracheal fluid of infants with CLD was less than 5 pg/ml. None of the infants with IL10 greater than 5 pg/ml developed CLD. The range of IL10 concentrations in tracheal fluid from infants without CLD was wide (0–938 pg/ml). There was no apparent correlation between IL10 levels and percentage neutrophil apoptosis in infants without CLD.
Conclusion: Preterm infants with low levels of IL10 and neutrophil apoptosis may be predisposed to disordered lung repair. Further studies into the method of disposal of senescent neutrophils within preterm lungs are required.
- chronic lung disease
- interleukin 10
- CLD, chronic lung disease
- IL, interleukin
- HMD, hyaline membrane disease
- MAS, meconium aspiration syndrome
- TNF, tumour necrosis factor
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