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Acute lung injury in preterm fetuses and neonates: mechanisms and molecular pathways.

Abstract Acute lung injury (ALI) results in high morbidity and mortality among preterm neonates and efforts have therefore been devoted to both antenatal and postnatal prevention of the disease. ALI is the result of an inflammatory response which is triggered by a variety of different mechanisms. It mostly affects the fetal lung and, in particular, causes damage to the integrity of the lung's alveolar-capillary unit while weakening its cellular linings. Chemotactic activity and inflammatory products, such as proinflammatory cytokines TNF-α, IL-1, IL-6, IL-11, VEGF,TGF-α and TGF-β, provoke serious damage to the capillary endothelium and the alveolar epithelium, resulting in hyaline membrane formation and leakage of protein-rich edema fluid into the alveoli. Chorioamnionitis plays a major part in triggering fetal lung inflammation, while mechanical ventilation, the application of which is frequently necessary in preterm neonates, also causes ALI by inducing proinflammatory cytokines. Many different ventilation-strategies have been developed in order to reduce potential lung injury. Furthermore, tissue injury may occur as a result of injurious oxygen by-products (Reactive Oxygen Species, ROS), secondary to hyperoxia. Knowledge of the inflammatory pathways that connect intra-amniotic inflammation and ALI can lead to the formulation of novel interventional procedures. Future research should concentrate on the pathophysiology of ALI in preterm neonates and οn possible pharmaceutical interventions targeting prevention and/or resolution of ALI.
PMID
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Authors

Mayor MeshTerms

Infant, Premature

Keywords
Journal Title the journal of maternal-fetal & neonatal medicine : the official journal of the european association of perinatal medicine, the federation of asia and oceania perinatal societies, the international society of perinatal obstetricians
Publication Year Start




PMID- 23611524
OWN - NLM
STAT- MEDLINE
DA  - 20131018
DCOM- 20140701
IS  - 1476-4954 (Electronic)
IS  - 1476-4954 (Linking)
VI  - 26
IP  - 17
DP  - 2013 Nov
TI  - Acute lung injury in preterm fetuses and neonates: mechanisms and molecular
      pathways.
PG  - 1696-704
LID - 10.3109/14767058.2013.798284 [doi]
AB  - Acute lung injury (ALI) results in high morbidity and mortality among preterm
      neonates and efforts have therefore been devoted to both antenatal and postnatal 
      prevention of the disease. ALI is the result of an inflammatory response which is
      triggered by a variety of different mechanisms. It mostly affects the fetal lung 
      and, in particular, causes damage to the integrity of the lung's
      alveolar-capillary unit while weakening its cellular linings. Chemotactic
      activity and inflammatory products, such as proinflammatory cytokines TNF-alpha, 
      IL-1, IL-6, IL-11, VEGF,TGF-alpha and TGF-beta, provoke serious damage to the
      capillary endothelium and the alveolar epithelium, resulting in hyaline membrane 
      formation and leakage of protein-rich edema fluid into the alveoli.
      Chorioamnionitis plays a major part in triggering fetal lung inflammation, while 
      mechanical ventilation, the application of which is frequently necessary in
      preterm neonates, also causes ALI by inducing proinflammatory cytokines. Many
      different ventilation-strategies have been developed in order to reduce potential
      lung injury. Furthermore, tissue injury may occur as a result of injurious oxygen
      by-products (Reactive Oxygen Species, ROS), secondary to hyperoxia. Knowledge of 
      the inflammatory pathways that connect intra-amniotic inflammation and ALI can
      lead to the formulation of novel interventional procedures. Future research
      should concentrate on the pathophysiology of ALI in preterm neonates and omicronn
      possible pharmaceutical interventions targeting prevention and/or resolution of
      ALI.
FAU - Iliodromiti, Zoe
AU  - Iliodromiti Z
AD  - 2nd Department of Obstetrics and Gynecology, University of Athens Medical School,
      Aretaieio Hospital , Athens , Greece .
FAU - Zygouris, Dimitrios
AU  - Zygouris D
FAU - Sifakis, Stavros
AU  - Sifakis S
FAU - Pappa, Kalliopi I
AU  - Pappa KI
FAU - Tsikouras, Panagiotis
AU  - Tsikouras P
FAU - Salakos, Nikolaos
AU  - Salakos N
FAU - Daniilidis, Angelos
AU  - Daniilidis A
FAU - Siristatidis, Charalambos
AU  - Siristatidis C
FAU - Vrachnis, Nikolaos
AU  - Vrachnis N
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20130520
PL  - England
TA  - J Matern Fetal Neonatal Med
JT  - The journal of maternal-fetal & neonatal medicine : the official journal of the
      European Association of Perinatal Medicine, the Federation of Asia and Oceania
      Perinatal Societies, the International Society of Perinatal Obstetricians
JID - 101136916
SB  - IM
MH  - Acute Lung Injury/epidemiology/*etiology
MH  - Female
MH  - Fetal Diseases/epidemiology/*etiology
MH  - Fetus
MH  - Humans
MH  - Infant, Newborn
MH  - *Infant, Premature
MH  - Lung/embryology/growth & development
MH  - Pregnancy
MH  - Premature Birth/epidemiology
MH  - Risk Factors
MH  - Signal Transduction/genetics
EDAT- 2013/04/25 06:00
MHDA- 2014/07/02 06:00
CRDT- 2013/04/25 06:00
PHST- 2013/05/20 [aheadofprint]
AID - 10.3109/14767058.2013.798284 [doi]
PST - ppublish
SO  - J Matern Fetal Neonatal Med. 2013 Nov;26(17):1696-704. doi:
      10.3109/14767058.2013.798284. Epub 2013 May 20.

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