R Henry

Publications (3)7.77 Total impact

• Article: Early postnatal surge of serum Clara cell secretory protein in newborn infants.

  A S Loughran-Fowlds, J W Lin, J Oei, J Michalowski, R Henry, K Lui
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  ABSTRACT: Clara cell secretory protein (CCSP) is an anti-inflammatory mediator, but its role in neonatal lung adaptation and diseases is uncertain. To characterize postnatal changes in serum CCSP in relation to gestation, respiratory disease (RDS) and bronchopulmonary dysplasia (BPD) in comparison with other anti-inflammatory cytokines (IL-4, -10 and -13). Blood was collected from 76 infants (26 of 23-29 weeks' gestation, 33 of 30-36 weeks' gestation and 17 term infants) at birth (preterm cord blood); on admission; at 12, 24 and 48 h; and on days 3-4 and 7 of life. CCSP was assayed by ELISA and cytokines by Bio-Plex. Median serum CCSP in extremely and moderately preterm infants rose from a baseline of 13.6 and 15.9 to 33.4 ng/ml (p = 0.04) and 59.8 ng/ml (p = 0.03) at 12 h of age, respectively. CCSP levels were highest in term infants (80.7 ng/ml at 12 h). CCSP then decreased to 22.5 ng/ml on days 3-4 (p = 0.001). CCSP of 37 RDS infants fell to a lower baseline on days 4 and 7 than that of the 22 non-RDS preterms. The 8 infants who developed BPD had persistently low serum CCSP (12.7 ng/ml at 12 h). In contrast, early postnatal changes were not seen in IL-4, -10 and -13 levels, but low IL-10 and -13 levels were found on day 7 in BPD infants. Serum CCSP levels were characterized by an early postnatal surge. This apparent gestation-influenced surge may represent an initiation of a protective cascade against postnatal lung injury during extrauterine adaptation.
  Neonatology 09/2011; 101(2):125-31. · 2.66 Impact Factor
• Article: Decreased neutrophil apoptosis in tracheal fluids of preterm infants at risk of chronic lung disease.

  J Oei, K Lui, H Wang, R Henry
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  ABSTRACT: 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. Prospective cohort design. 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). 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. 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.
  Archives of Disease in Childhood - Fetal and Neonatal Edition 06/2003; 88(3):F245-9. · 3.05 Impact Factor
• Article: Decreased interleukin-10 in tracheal aspirates from preterm infants developing chronic lung disease.

  J Oei, K Lui, H Wang, R Henry
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  ABSTRACT: The inability to balance pulmonary injury with healing may predispose preterm infants to chronic lung disease (CLD). It is postulated that the production of interleukin (IL)-10, an anti-inflammatory cytokine, is gestationally influenced and that CLD-prone infants may have a reduced ability to produce IL-10. Tracheal fluid (TF) was collected at least twice weekly from 48 mechanically ventilated infants within the first 7 d of life while intubated. A total of 87 TF specimens were obtained. None of the 11 CLD infants (24-31 wk of gestation) had TF IL-10 levels above 4 pg/ml (0/20 TF specimens), while 14 (70%) of the 20 non-CLD preterm infants (27-36 wk of gestation) had IL-10 levels above 5 pg/ml in one or more of their TF specimens (18/48 TF specimens, p < 0.001). Only the 5 term infants who were ventilated for severe lung disease had raised IL-10 levels (17 infants, 5/19 TF specimens). IL-10 levels, if detected, (range 6-938 pg/ml) tended to be higher with increasing gestation (Spearman's rho coefficient = 0.43; p = 0.003). TF IL-10 detection was not associated with hyaline membrane disease, antenatal steroids or influenced by TF sample volume. Overall IL-8 levels were wide ranging but towards the end of week 1 the levels were significantly higher in CLD infants (CLD: median 34 184 ng/ml, preterm non-CLD: median 699 ng/ml, p < 0.001, term: 2961 ng/ml, p = 0.028). A gestationally influenced low IL-10 may predispose preterm infants to persistent pulmonary inflammation of CLD.
  Acta Paediatrica 02/2002; 91(11):1194-9. · 2.07 Impact Factor