الفهرس 
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Abstract
Clara cells and human Clara cell protein (CCSP) belongs to the family of
secretoglobins, it is a secreted protein product of non- ciliated tracheal and bronchiolar Clara
cell.
It is now recognized that epithelial cells lining airways and alveoli are capable of
releasing various mediators, which have the potential to modulate local inflammatory reaction
like Clara cell protein which appears to protect the respiratory tract against oxidative stress
and inflammation.
In vitro, CC16 has been shown to modulate the production and/or the activity of various
mediators of the inflammatory response including PLA2, interferon-gamma and tumor
necrosis factor-alpha. CC16 has also been found to inhibit fibroblast migration or to bind
various endogenous or exogenous substances such as polychlorobiphenyls (PCBs).
CCSP presents a major interest as a peripheral marker for assessing the integrity of the
lung epithelium. The determination of CC16 in plasma is a non-invasive test to detect Clara
cell damage or an increased epithelial permeability in various acute and chronic lung
disorders.
In this study, our goal was to examine the early postnatal behavior of CC16 in newborn
plasma and broncho- alveolar lavage fluid as an inflammatory lung mediator in the lung in
relation to Apgar score, weight, gestation, respiratory disease & sepsis and to examine the
pattern of this protein in serum protein electrophoresis in preterm & full term neonates.
The current study included 64 neonates with range of age (1 – 3 days), 39
males and 25 females.
Plasma samples were 55 samples from neonates aged 1 day; the remaining 9
samples were endo-tracheal broncho-alveolar lavage for mechanically ventilated
neonates ranged from (1 – 3 days). Samples were collected from January 2011 to
June 2011.
Thirty four of neonates were full term babies , their gestational age ranged from
(37 – 40 week), 5 of neonates were post term with gestational age ranged more than 42
weeks, 25 of neonates were preterm babies, their gestational age ranged from (27 – 37
week), 2 of them were ELBW (Extremely low birth weight), their gestational age
ranged 27 weeks.
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All neonates were subjected to:
Apgar Score including (Heart rate, Breathing, Grimace, Activity (muscle tone),
Skin coloration).
Clinical examination.
Laboratory investigations which includes
1 – Hemoglobin
2 – CRP
3- CCSP
4 – Protein electrophoresis.
In our study preterm neonates, regardless of lung disease, showed a significant
reduction in plasma levels of Clara cell secretory protein in comparison to full term
neonates. Also, there was a positive correlation between gestational age and Clara cell
secretory protein in plasma group.
There was a significant increase in Clara cell secretory protein levels in neonates
regardless of gestation, with acute lung injury (pneumonia, sepsis) more than CRP in
healthy neonates. Also, there was a decrease of Clara cell secretory protein in neonates
with respiratory distress & in cases of lung immaturity. Moreover, there was correlation
between different grades of respiratory distress & Clara cell protein in plasma group.
In the present study, we found that there was reduction in Clara cell secretory protein in
BAL of mechanically ventilated preterm in comparison to mechanically ventilated full term
neonates, and there was a correlation between gestational age and Clara cell secretory protein
in broncho alveolar lavage fluid. But there was no obvious results have been reported as
regards the measurement of Clara cell protein in broncho- alveolar lavage fluid in neonates
with infection.
Finally in our study, neonates were subjected to serum protein electrophoresis which
reported normal values of different protein fractions & showed normal protein electrophoresis
pattern in both preterm & full term neonates.