PMID- 16188792
OWN - NLM
STAT- MEDLINE
DCOM- 20051014
LR  - 20191210
IS  - 0803-5253 (Print)
IS  - 0803-5253 (Linking)
VI  - 94
IP  - 6
DP  - 2005 Jun
TI  - Inflammatory chemokine expression in the peripheral blood of neonates with 
      perinatal asphyxia and perinatal or nosocomial infections.
PG  - 800-6
AB  - AIM: The inflammatory response induced by perinatal infections and asphyxia is 
      considered to participate in neonatal brain damage. Inflammatory responses are 
      characterized by the expression of chemokines. Although chemokine levels have 
      been investigated in healthy newborns, their role during neonatal pathological 
      conditions has not been studied. The aim of our study was to examine chemokine 
      serum levels in asphyxiated and infected neonates. METHODS: Peripheral blood 
      samples were obtained from perinatally asphyxiated and infected neonates during 
      the first days of life and from neonates who developed nosocomial infections. 
      Serum levels of interleukin-8 (IL-8), interferon-gamma-inducible protein-10 
      (IP-10), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory 
      protein-1alpha (MIP-1alpha), and regulated upon activation, normal T cells 
      expressed and secreted (RANTES) were determined. RESULTS: In perinatally 
      asphyxiated neonates, IL-8 levels were significantly elevated on the 1st day of 
      life. In perinatally infected neonates, IL-8 and IP-10 levels were significantly 
      increased on the 1st day of life, while RANTES levels were significantly lower 
      and remained so until the 4th day. In nosocomially infected neonates, IL-8, IP-10 
      and MIP-1alpha levels were significantly increased on diagnosis of infection. 
      CONCLUSION: The neonatal immune system is able to produce chemokines for the 
      induction of an inflammatory response during perinatal asphyxia and perinatal or 
      nosocomial infections. Blockade of inflammatory chemokines could possibly 
      contribute to the prevention of brain damage.
FAU - Fotopoulos, Spyros
AU  - Fotopoulos S
AD  - Neonatal Intensive Care Unit B, Aghia Sophia Children's Hospital, Athens, Greece.
FAU - Mouchtouri, Alexia
AU  - Mouchtouri A
FAU - Xanthou, Georgina
AU  - Xanthou G
FAU - Lipsou, Niki
AU  - Lipsou N
FAU - Petrakou, Eftichia
AU  - Petrakou E
FAU - Xanthou, Marietta
AU  - Xanthou M
LA  - eng
PT  - Journal Article
PL  - Norway
TA  - Acta Paediatr
JT  - Acta paediatrica (Oslo, Norway : 1992)
JID - 9205968
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Chemokine CXCL10)
RN  - 0 (Chemokines)
RN  - 0 (Interleukin-8)
RN  - 0 (Macrophage Inflammatory Proteins)
SB  - IM
MH  - Asphyxia Neonatorum/*blood
MH  - Chemokine CCL2/blood
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Chemokine CCL5/blood
MH  - Chemokine CXCL10/blood
MH  - Chemokines/*blood
MH  - Cross Infection/*blood
MH  - Humans
MH  - Infant, Newborn
MH  - Infections/*blood
MH  - Interleukin-8/blood
MH  - Macrophage Inflammatory Proteins/blood
EDAT- 2005/09/29 09:00
MHDA- 2005/10/15 09:00
CRDT- 2005/09/29 09:00
PHST- 2005/09/29 09:00 [pubmed]
PHST- 2005/10/15 09:00 [medline]
PHST- 2005/09/29 09:00 [entrez]
AID - P220075848662667 [pii]
AID - 10.1111/j.1651-2227.2005.tb01988.x [doi]
PST - ppublish
SO  - Acta Paediatr. 2005 Jun;94(6):800-6. doi: 10.1111/j.1651-2227.2005.tb01988.x.