ABSTRACT Clara cell secretory protein (CC10) is an important anti-inflammatory mediator in the adult lung, but its role in newborn pulmonary protection is uncertain. We examined the early

postnatal behavior of CC10 in newborn serum and tracheal fluid and hypothesized that CC10 production is positively influenced by gestation. Blood from 165 infants from the first,

third/fourth, and seventh days of life (gestational ages: 23–29 wk, 30–36 wk, >36 wk) and tracheal fluid (TF) from the first day of life from 32 ventilated infants were analyzed for CC10.

Surfactant proteins A (SPA) and B (SPB) were also analyzed from the blood of a subgroup of infants. Serum CC10 on day 1 was highest in term infants (69.4 ng/mL), followed by moderately

decreased progressively by the end of the first week in all infants, in contrast to SPA and SPB, which increased. Our results show that CC10 is detectable in the blood of newborn infants and

that a production surge occurs at birth. This surge is more pronounced in term infants and may confer them with superior extrauterine pulmonary protection compared with preterm infants.

SIMILAR CONTENT BEING VIEWED BY OTHERS EFFICACY OF SYNTHETIC SURFACTANT (CHF5633) BOLUS AND/OR LAVAGE IN MECONIUM-INDUCED LUNG INJURY IN VENTILATED NEWBORN RABBITS Article 14 June 2022

EFFECT OF THERAPEUTIC HYPOTHERMIA ON SURFACTANT PROTEINS, ANTI-INFLAMMATORY AND PRO-FIBROTIC MEDIATORS Article 02 April 2025 BLOOD METABOLOMICS IN INFANTS ENROLLED IN A DOSE ESCALATION PILOT

TRIAL OF BUDESONIDE IN SURFACTANT Article 19 January 2021 MAIN There has been little impact on the severity and incidence of chronic lung disease (CLD) despite considerable advances in

perinatal care (1). The etiology of CLD, a syndrome of persistent respiratory insufficiency in which preterm infants continue to require supplemental oxygen and/or mechanical ventilatory

support beyond the postconceptional age of 36 wk (2), remains uncertain, but there is increasing evidence to suggest that premature infants are unable to temper the inflammatory response

caused by extrauterine insults such as mechanical ventilation, sepsis, and oxygen (3). An early increase of cellular and humoral inflammatory mediators (4,5), as well as a concomitant

decrease in protective antiprotease, antioxidant, surfactant, and anti-inflammatory systems (6), has been noted soon after birth in lung fluids of infants who subsequently developed CLD.

Recently, the 16-kD lung-specific anti-inflammatory protein, CC10 (known as CCSP, uteroglobin, or CC16), produced by nonciliated bronchiolar lung Clara cells, was shown to play a pivotal

role in the prevention and amelioration of lung injury in adult mice and humans (7–9). Its effects on the newborn lung, however, are uncertain. The amniotic fluid and TF concentrations of

CC10 increase with advancing gestational age (10–12), but whether this is a true representation of a gestational effect on CC10 production is questionable. For example, amniotic fluid

studies, although involving large numbers of pregnancies, are predominantly composed of subjects with problematic and genetically abnormal pregnancies (10,11). Lung fluid studies, on the

other hand, are usually small (12) and include only ventilated infants. The CC10 profile of normal infants is therefore not easily examined by either of these studies. Fortunately, CC10 is

detectable in serum because it leaks passively from the lungs into the circulation through the bronchoalveolar blood barrier (13), and serum CC10 may therefore be used as a surrogate

representative of lung CC10. Serum CC10 has not been comprehensively studied in the neonatal population. There are also currently no data on gestational influence on serum CC10, and in this

study, we sought to examine whether 1) CC10 was detectable in neonatal blood, 2) gestation and pulmonary outcome influences CC10 concentrations, and 3) there was any relationship between

CC10 and the behavior of other pneumoproteins such as SPA and SPB. We hypothesize that early production of CC10 during extrauterine adaptation is influenced by gestation. Additionally, our

secondary hypothesis is that full-term infants will have higher concentrations of CC10 in both serum and TFs than premature infants at high risk of developing CLD. METHODS The infants in

this study were recruited from the neonatal intensive care unit at the Royal Hospital for Women in Randwick, Australia, between June 2001 and December 2003. Infants were eligible for the

study if they were less than 24 h of age at time of enrollment and if they required blood tests as part of routine medical management. Infants with major chromosomal anomalies, congenital

anomalies of the lungs, or pulmonary hypoplasia were excluded. The infants were divided into three gestational cohorts consisting of extremely premature infants (23–29 wk gestation),

moderately premature infants (30–36 wk gestation), and term infants (>36 wk gestation). We obtained 0.5 mL of blood (by venous, arterial, or heel puncture) from each infant on d 1, 3–4,

and 7 of life. Blood sampling was timed to coincide with medically indicated blood tests. D 7 specimens were not collected in term infants because most had been discharged from hospital by

that time. Investigations were extended to include SPA and SPB assays during a later part of the study, in which an extra 0.2 mL of blood was obtained from consecutively enrolled infants for

SPA and SPB measurement. TFs were collected from mechanically ventilated infants on the first day during routine pulmonary toilet: 0.5 mL of saline was instilled in the endotracheal tube

and the residue suctioned after two to three ventilator breaths (6). All specimens were immediately spun in an on-site laboratory for 10 min at 3500 RPM and the supernatant frozen and stored

at –70°C until analysis. CC10 was assayed in serum and TF in batches of 40 in duplicates by a commercially available CC10 enzyme-linked immunosorbent assay (ELISA) (DIAMED, Belgium) (14).

This uses anti-monoclonal antibody for quantitative determination of CC10. CC10 is then bound to specific biotin-conjugated antibodies, and the amount present is detected by addition of

streptavidin–horseradish peroxidase, hydrogen peroxide, and tetramethylbenzidine buffer solution. Absorbency is measured at 450 nm and standard curves generated to determine CC10

concentrations. Detection limits are 0.03 ng/mL. The intra- and interassay coefficients of variation of the method are less than 4% at a level of 0.1 ng/mL and less than 3% at a level of 3

ng/mL (15). We confirmed in our laboratory that the CCSP standards used in the ELISA kit were of the same molecular weight as the recombinant human CC10 (rhCC10) (courtesy of April Pilon,

Claragen, Baltimore, MD) and verified by Western blot that the ELISA kit antibodies recognized rhCC10. CC10 assay values were expressed as weight per volume lavage fluid because an

acceptable method for standardizing solute quantities in pulmonary lavage specimens has not been well established (16). Serum SPA and SPB were measured in duplicate at four serial dilutions

with ELISA inhibition assays by Flinders University, Adelaide, using previously established methods (17). Briefly SPA and SPB were first freed from any associated components using

ethylenediaminetetraacetic acid, sodium dodecylsulfate, and Triton X-100. The proteins were then measured with ELISA inhibition assays using polyclonal antibodies raised against alveolar

proteinosis–derived SPA and mature SPB, respectively. Absorbance was measured at 405 nm, and standard curves were generated to compute the concentration in each sample. Demographic details

recorded included antenatal steroids, maternal cigarette exposure, pregnancy and delivery histories, resuscitation, and ventilatory parameters. Respiratory disease was diagnosed clinically

and radiologically and included respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN), and other respiratory disorders. Infants with respiratory disease were treated

according to nursery protocol, which included mechanical ventilation and oxygen for most extremely premature infants and continuous positive airway pressure for less premature infants with

mild disease. Survanta®, which contains SPB but not SPA, was used in treatment of radiologically diagnosed RDS. Neonatal outcomes examined included mortality and the development of CLD,

which was defined as the need for supplemental oxygen and/or ventilatory support at and beyond the postconceptional age of 36 wk in premature infants (2). No infant received steroids during

the period of sample collection. Variance of serum CC10 concentrations, obtained from a pilot sample of 28–32 wk gestation infants, was used for sample size calculations. This showed that 19

infants were required in each group to demonstrate adequate differences (to test for a mean difference of 5 ng/mL, alpha = 0.01, power = 0.90, two-tailed test). Categorical data were

analyzed by Fisher's exact test and/or χ2 test. Nonparametric analyses were used (Mann-Whitney _U_, Kruskal-Wallis, Friedman, Spearman's rho, and Wilcoxon). A _p_ < 0.05 was

considered significant. No infants were excluded from overall analyses but were excluded from CLD analysis if they died before 36 wk gestational age. The Institutional Ethics Committee of

the South East Sydney Area Health Service approved the study and signed informed consent was obtained from each infant's parents. RESULTS Blood samples (_N_ = 312) were collected from

165 infants. Sixty were extremely premature (23–29 wk gestation; median 27 wk), 66 were moderately premature (30–36 wk gestation; median 33 wk), and 39 were full term (median 40 wk);

demographic characteristics are summarized in Table 1. Only six term infants remained in the nursery by the end of the first week of life and therefore, d 7 blood results from this group

were not included in our analysis. Investigations were extended in a later part of the study to include collection of an extra 0.2 mL of blood from a consecutive subpopulation of 41 infants

(14 extremely preterm, 19 moderately preterm, and eight term) for serum SPA (97 samples) and SPB (95 samples) measurement. There was no difference in the demographics of the two groups.

RELATIONSHIP BETWEEN GESTATION, POSTNATAL AGE, AND SERUM CC10. The first collection of blood occurred at a median of 12 h (interquartile range: 3–19 h] after birth for all groups. D 1 CC10

concentrations were significantly influenced by gestation, being lowest in extremely preterm infants [median 42.1 ng/mL (17.2, 57.8)], followed by moderately preterm infants [55.8 ng/mL

(26.0, 73.9)], and highest in term infants [69.4 ng/mL (59.6, 73.8); _p_ = 0.005]. Subsequent serum CC10 concentrations stayed relatively stable in extremely preterm infants [d 4: 32.7 ng/mL

(15.7, 51.6); d 7: 26.8 ng/mL (17.5, 44.6); _p_ = 0.738] but fell significantly in the other two groups in comparison with d 1 [moderately preterm d 4: 31.2 ng/mL (19.0, 61.4); d 7: 28.9

ng/mL (14.7, 56.2), _p_ = 0.004; term d 4: 25.2 ng/mL (15.4, 55.8); d 7: 23.9 ng/mL (13.7l, 34.0), _p_ = 0.006] (Fig. 1). RELATIONSHIP BETWEEN GESTATION AND TF CC10. Of the 165 infants, 89

were ventilated and therefore eligible for TF collection. This was limited to office hours because of laboratory staff availability (samples had to be spun within an hour of collection). TF

was collected from 49 infants on d 1, but 17 were rejected for testing because of an unsuitably small volume of return (less than 100 μL) (6). TFs were analyzed in 32 infants: 18 extremely

premature, five moderately premature, and nine full term. There were no overall demographic biases between sampled infants and nonsampled ventilated infants. TF CC10 on d 1 correlated

positively with gestation (Spearman's rho correlation coefficient 0.410, _p_ < 0.020). The median concentration in preterm infants was 882 ng/mL (442, 2655) [compare term infants:

20,152 ng/mL (724, 43, 112), _p_ = 0.022]. POSTNATAL BEHAVIOR OF SERUM SPS. D 1 serum SPA concentrations from the subgroup of 41 infants (Fig. 2) were similar to those of serum CC10.

Extremely preterm infants had lowest concentrations [0.7 μg/mL (0.6, 2.3)] followed by moderately preterm infants [1.0 μg/mL (0.6, 1.3)] and then term infants [1.1 μg/mL (0.67, 1.6), _p_ =

0.958]. However, SPA concentrations rose on d 4 in all gestations, and this increase was most pronounced in more mature infants [0.8 μg/mL (0.6, 1.4), 1.3 μg/mL (0.9, 1.9), and 1.9 μg/mL

(1.6, 2.4), respectively; _p_ = 0.008]. Ten (24%) of the 41 infants had RDS, and all received surfactant treatment before collection of the d 1 samples. Serum SPB varied more greatly than

SPA, but no observable differences were seen in serum SPB between the gestational groups: extremely preterm: 10.7 μg/mL (6.9, 18.3), moderately preterm: 10.2 μg/mL (6.5, 16.8), and term: 9.5

μg/mL (3.1, 14.5) (_p_ = 0.757). Serum SPB increased by almost twofold on d 4, but there was no apparent gestational influence (Fig. 2): 21.8 μg/mL (13.2, 33.5), 16.1 μg/mL (13.6, 22.9),

and 15.3 μg/mL (10.7, 23.0), respectively (_p_ = 0.919). INFLUENCE OF VENTILATION AND RDS ON SERUM CC10 IN CORRESPONDING GESTATION GROUPS. Only four extremely premature infants did not

require ventilatory support, 80% had RDS, and all but one were treated with Survanta®. Infants treated with Survanta® did not have statistically different concentrations of CC10 compared

with those untreated [extremely preterms: d 1: 44.8 ng/mL (15.0, 63.2) _versus_ 30.2 ng/mL (21.2, 55.2), _p_ = 0.742; d 4: 24.2 ng/mL (15.6, 52.6) _versus_ 37.6 ng/mL (28.6, 48.3), _p_ =

0.519; moderately preterm: d 1: 55.4 ng/mL (43.3, 71.6) _versus_ 55.2 ng/mL (24.7, 73.9), _p_ = 0.739; d 4: 31.5 ng/mL (14.2, 38.3) _versus_ 34.5 ng/mL (19.6, 65.4), _p_ = 0.297).Ventilated

infants had slightly higher d 1 serum CC10 than nonventilated infants [44.9 ng/mL (18.4, 60.5) _versus_ 24.2 ng/mL (18.3, 27.2); _p_ = 0.257]. Concentrations were also slightly higher in the

48 infants with RDS compared with infants without RDS on d 1 [49.3 ng/mL (16.0, 69.8) _versus_ 12 non-RDS 24.0 ng/mL (20.8, 30.2), _p_ = 0.307], but concentrations on d 4 and 7 were not

different between the groups. These differences were most marked in moderately preterm infants, in whom ventilation was associated with considerably higher d 1 CC10 concentrations [24

ventilated: 66.1 ng/mL (50.9, 78.5) _versus_ 32 nonventilated: 41.8 ng/mL (23.9, 71.2); _p_ = 0.013] (Fig. 3). Moderately preterm infants with RDS, however, had CC10 concentrations similar

to those without RDS on d 1 of life [22 RDS infants: 55.4 ng/mL (43.1, 71.8) _versus_ 44 non-RDS infants: 56.2 ng/mL (25.0, 74.7), _p_ = 0.173]. There was no difference in CC10

concentrations between ventilated and nonventilated term infants [ventilated: 70.8 ng/mL (58.6, 82.4) _versus_ nonventilated: 69.4 ng/mL (59.6, 73.8); _p_ = 0.682]. The influence of RDS in

this group was not analyzed because only one infant had RDS. Maternal antenatal steroid treatment was examined as a confounder and was found to be an insignificant first day influence on

preterm serum CC10 [extremely preterm maternal steroid: 42.1 ng/mL (15.7, 57.7) _versus_ no maternal steroid: 55.7 ng/mL (24.0, 116.0), _n_ = 53 (88%): _p_ = 0.266; moderately preterm 56.9

ng/mL (39.5, 72.4) _versus_ 55.5 ng/mL (24.7, 74.4), _n_ = 31 (47%): _p_ = 0.876]. Smoking history was obtained for mothers of 132 infants. Smoking did not influence serum CC10 on any days

[E.G. d 1: extremely preterm exposed: 55.2 ng/mL (22.0, 66.5) _versus_ not exposed: 34.9 ng/mL (14.9, 56.2), _n_ = 11 (22%), _p_ = 0.634; moderately preterm exposed: 74.7 ng/mL (61.6, 77.3)

_versus_ not exposed: 57.3 ng/mL (36.5, 78.8), _n_ = 7 (11%), _p_ = 0.278; term exposed: 88.7 ng/mL (59.4, 118.1) _versus_ not exposed: 69.3 ng/mL (57.9, 76.0), _n_ = 4 (10%), _p_ = 0.766].

RELATIONSHIP BETWEEN SERUM CC10 AND CLD. Only one (2%) moderately preterm infant developed CLD. Fifteen (25%) of the 23–29 wk infants died, two from respiratory failure and one from

pulmonary hemorrhage. Most deaths were from nonrespiratory causes, including intraventricular hemorrhages (_n_ = 7), necrotizing enterocolitis (_n_ = 2), meconium peritonitis (_n_ = 1),

hypotension (_n_ = 1), and sepsis (_n_ = 1). All the deaths occurred before 36 wk postconceptional age, and hence infants were excluded from analyses involving CLD. Fourteen (23%) infants

developed CLD. All CLD infants and 19 of the 31 non-CLD infants were ventilated. Serum CC10 was slightly, but not significantly, lower on d 1 and 4 in CLD infants [d 1: 15.0 ng/mL (11.6,

72.4) _versus_ 37.7 ng/mL (21.5, 56.2), _p_ = 0.500; d 4: 21.6 ng/mL (15.2, 31.0) _versus_ 33.8 ng/mL (22.5, 48.3), _p_ = 0.201] (Fig. 4).). A stronger trend was obtained if respiratory

deaths were included in the analysis of CLD [d 1: 14.7 ng/mL (11.0, 72.2) _versus_ 49.4 ng/mL (24.1, 57.8), _p_ = 0.116; d 4: 20.4 ng/mL (14.1, 29.0) _versus_ 37.4 ng/mL (22.7, 57.2), _p_ =

0.068]. RELATIONSHIP BETWEEN SERUM PNEUMOPROTEINS AND RENAL FUNCTION. Serum CC10, SPA, and SPB were analyzed in conjunction with serum creatinine to determine the effects of renal function.

All proteins showed no significance on d 1, 4, and 7 when compared with serum creatinine. DISCUSSION To our knowledge, this is the first study to comprehensively demonstrate the behavior of

serum CC10 in newborn infants during the first week of life. Apart from a small renal contribution, the majority of CC10 originates from the lungs (18), and one can assume that the CC10 that

we analyzed from blood was a result of passive diffusion from the lungs to the circulation. Only minute amounts of CC10 cDNA have been found in human placentas and uteruses (19); therefore,

it is unlikely that maternal contribution would be significant. Our results suggest that extremely preterm infants, especially those prone to CLD, produce less pulmonary CC10 than more

mature infants with a good pulmonary outcome. Differences in CC10 production may be vital in postnatal extrauterine pulmonary adaptation and in the development of the type of lung injury

frequently associated with lung immaturity. CC10 is anti-inflammatory and inhibits phospholipase A2 (PLA2) activity (7), the production and function of interferon-γ (9), and the chemotaxis

of fetal lung fibroblasts (7). The importance of CC10 in preventing lung injury has been demonstrated in genetically modified CC10-deficient mice, which have an increased sensitivity and

exaggerated inflammatory response to lipopolysaccharide and hyperoxic or ozone-induced lung injury (20). All the newborn infants in our study, regardless of lung disease, had much higher

concentrations of serum CC10 than healthy adults (9–21 ng/mL) (21). Such concentrations may be necessary for acute postnatal lung adaptation. However, excessively elevated concentrations may

also be an indication of a disrupted or underdeveloped bronchoalveolar blood barrier. For example, adults and animals with inflammatory lung disease and damaged pulmonary barriers have

increased leakage of CC10 from the lungs into the circulation, as indicated by _decreased_ pulmonary effluent and _increased_ serum concentrations of CC10 (22). In our study, higher

concentrations of serum CC10 in ventilated preterm infants may have been due to be a disruption of the bronchoalveolar blood barrier, either from lung disease or mechanical ventilation or

from an underdeveloped barrier in extremely premature infants, but our TF studies confirmed that CC10 concentrations were, indeed, higher with increasing maturity. We found that the

postnatal behavior of serum CC10 was different from that demonstrated by the SPs; the latter increased toward the end of the first week instead of decreasing. The difference in behavior was

not due to selection bias because a comparison of demographics showed no significant differences. This difference also cannot be solely explained by leakage because SPB is of a molecular

size similar to that of CC10. The half-life of all three proteins in the circulation is less than 18 min (23), therefore discounting this as a factor. The lack of gestational influence on

serum SPA was an unexpected finding because fetal lung SPA has been shown to increase with advancing gestation (24). The molecular weight of SPA (35 kD) is considerably larger than that of

CC10, and SPA may therefore be more confined to the intravascular space and not as dependent on glomerular filtration for clearance (23). However, we may have documented a difference in the

behavior of serum SPA had we had obtained blood from more infants. A gestational influence on CC10 production has been suggested by previous studies on amniotic fluid and TF of mechanically

ventilated premature infants (10–12). CC10 is detectable in amniotic fluid from 15 wk of gestation (10) and increases with advancing gestation, possibly due to fetal airway growth (10,11).

In a cross-sectional study of ventilated premature infants during the first 2 wk of life (median gestation 27.9 wk), CC10 concentrations in TF increased with both postnatal age and gestation

(12). None of these studies, however, explored early postnatal changes. We studied infants from a wider gestational range and our longitudinal analysis included both nonventilated and

healthy infants. Our results showed that term infants who are better equipped for extrauterine life had highest serum and TF CC10 on d 1; these new findings indicate that CC10 production at

birth may be an important part of postnatal adaptation. The influence of mechanical ventilation on serum CC10 concentration in premature infants is more difficult to delineate as this

parameter is confounded by the two most important influences on serum CC10 concentrations: gestation and RDS. These two factors are inversely interdependent and in the extremely premature

group, very few infants escaped mechanical ventilation and the majority had RDS. A small number had TTN and other disorders and were separated from the RDS group for analysis. In the

moderately premature group, however, RDS did not make a difference to serum CC10 concentrations, even though a difference was seen between the ventilated and nonventilated infants. These

results imply that CC10 production is independent of the surfactant system, as suggested by previous studies (11). Elevated serum CC10 in ventilated preterm infants may have been caused by

leakage through a damaged fragile preterm bronchoalveolar barrier. A proinflammatory response may have been incited by damage caused by mechanical ventilation, but this type of response

usually takes a few days to weeks (25) and is not usually evident on the first day of life, as seen in the CC10 changes in this study, where serum CC10 continued to fall despite continued

ventilation. We may not have found a demonstrably noticeable difference in serum CC10 between ventilated and unventilated term infants because of the heterogeneous variety of respiratory

disease in this group. More studies, particularly in animal models, are required to investigate this. This study also showed that CLD infants had the lowest serum CC10 concentrations

compared with gestationally similar infants. Although infants at risk of developing CLD are usually ventilated, have RDS, and receive surfactant, these factors are not prerequisites for the

development of CLD (26). When results for infants who died from respiratory causes were included in the analysis, serum concentrations of CC10 were even lower (although this difference was

not significant: _p_ = 0.068). The number of CLD infants in our cohort was small, and further studies with larger sample sizes of CLD-prone infants are required to explore the relationship

between low levels of CC10 and CLD. This finding has important therapeutic implications as recombinant CC10 has been shown to confer significant pulmonary protection in newborn infants and

animals (27,28). We expressed CC10 concentrations as weight per volume lavage TF because an acceptable method for standardizing solute quantities in TF specimens is not well established

(16). Adjustment for various markers can be performed; however, they have been found to be unreliable for the calculation TF dilution (29). Albumin is especially unsuitable as a denominator

as there is little relation between serum and TF concentrations (29,30), the latter being also subject to variation because of acute flux and disease activity (30), particularly in the

context of heterogeneous lung diseases in our study population. The magnitude of CC10 difference in TF was much higher than anticipated from the serum levels. This may suggest enhanced CC10

production in full-term infants in response to lung disease. In conclusion, our study has demonstrated that CC10 is detectable in blood of newborn infants and that production of CC10 is

highest on the first day of life. We have also demonstrated that CC10 production is correlated to gestational age and that the importance of CC10 as an anti-inflammatory pneumoprotein places

those with CC10 deficiency at possible risk of postnatal respiratory injury. CC10 production also appears independent of surfactant maturation, and further studies assessing the role of

CC10 in extrauterine adaptation are urgently needed. ABBREVIATIONS * CC10: Clara cell secretory protein * CLD: chronic lung disease * RDS: respiratory distress syndrome * SP: surfactant

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references ACKNOWLEDGEMENTS We thank the parents, newborn babies, and staff of the Department of Newborn Care at the Royal Hospital for Women for participating in this study and in

collecting samples; the South Eastern Area Laboratory Services, especially Assisant Professor Daya Naidoo and Dr. Ora Lux, for help with initial sample collation and storage; Drs. Ian Doyle

and Heather Barr, Flinders University, Adelaide, for performing surfactant protein assays and Andrew Fowlds for computer support. AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Department of

Newborn Care, Royal Hospital for Women, Randwick, 2031, NSW, Australia Alison Loughran-Fowlds, Julee Oei, Neil Wimalasundera & Claire Egan * Leslie Stevens Newborn Research Laboratory,

Royal Hospital for Women, Randwick, 2031, NSW, Australia Hongxiu Xu & Kei Lui * School of Women's and Children's Health, University of New South Wales, Randwick, 2031, NSW,

Australia Julee Oei, He Wang, Hongxiu Xu, Richard Henry & Kei Lui Authors * Alison Loughran-Fowlds View author publications You can also search for this author inPubMed Google Scholar *

Julee Oei View author publications You can also search for this author inPubMed Google Scholar * He Wang View author publications You can also search for this author inPubMed Google Scholar

* Hongxiu Xu View author publications You can also search for this author inPubMed Google Scholar * Neil Wimalasundera View author publications You can also search for this author inPubMed 

Google Scholar * Claire Egan View author publications You can also search for this author inPubMed Google Scholar * Richard Henry View author publications You can also search for this author

inPubMed Google Scholar * Kei Lui View author publications You can also search for this author inPubMed Google Scholar CORRESPONDING AUTHOR Correspondence to Julee Oei. ADDITIONAL

INFORMATION This study was supported by grants from the Leslie Stevens Fund for Newborn Care, Sydney Children's Hospital Foundation, and the Roth Foundation, Sydney, Australia. RIGHTS

AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Loughran-Fowlds, A., Oei, J., Wang, H. _et al._ The Influence of Gestation and Mechanical Ventilation on Serum

Clara Cell Secretory Protein (CC10) Concentrations in Ventilated and Nonventilated Newborn Infants. _Pediatr Res_ 60, 103–108 (2006). https://doi.org/10.1203/01.pdr.0000219388.56608.77

Download citation * Received: 02 August 2005 * Accepted: 09 February 2006 * Issue Date: 01 July 2006 * DOI: https://doi.org/10.1203/01.pdr.0000219388.56608.77 SHARE THIS ARTICLE Anyone you

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