Interleukin-8 and monocyte chemotactic protein-1 mRNA expression in perinatally infected and asphyxiated preterm neonates.
BACKGROUND
Inflammation due to perinatal infection (PI) and perinatal asphyxia (PA) may cause damage to various tissues and very often to the immature brain of the fetus and the newborn. Previously, we have shown that the neonatal immune system has the ability to produce increased chemokine protein levels in the serum during the inflammatory response caused by PI and PA.


OBJECTIVE
The aim of our present study was to investigate mRNA levels of the proinflammatory chemokines interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) in peripheral blood leukocytes from infected and asphyxiated neonates.


METHODS
Forty-two premature neonates were studied; 11 with PI, 16 with PA and 15 without PA and PI, were used as controls. IL-8 and MCP-1 mRNA levels were investigated in whole blood and in phytohemagglutinin-activated lymphocytes using semi-quantitative polymerase chain reaction and real-time polymerase chain reaction, respectively.


RESULTS
IL-8 mRNA levels were significantly increased in whole blood both during PA and PI, while MCP-1 mRNA levels were not. In vitro activated lymphocytes expressed significantly increased IL-8 mRNA levels during PI, whereas no increase was observed during PA. MCP-1 mRNA levels were significantly increased in activated lymphocytes during PA, while no increase was observed during PI.


CONCLUSIONS
Our data show that chemokine mRNA levels expressed by activated lymphocytes during inflammation caused by PIs are different to those expressed during PAs. These findings might have important implications during the administration of specific chemokine antagonists in order to prevent or reduce tissue damage caused by inflammation.
Petrakou
E
E
Neonatal Immunology Laboratory of B Neonatal Intensive Care Unit, Aghia Sophia Children's Hospital, Athens, Greece.
Mouchtouri
A
A
Levi
E
E
Lipsou
N
N
Xanthou
M
M
Fotopoulos
S
S
D001238:Asphyxia Neonatorum / Q000097:blood*; D018932:Chemokine CCL2 / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D003428:Cross Infection / Q000097:blood*; D015870:Gene Expression; D006801:Humans; D007231:Infant, Newborn; D016209:Interleukin-8 / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism*; D008213:Lymphocyte Activation; D008934:Mitogens / Q000494:pharmacology; D010835:Phytohemagglutinins / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism*
D018932:Chemokine CCL2; D016209:Interleukin-8; D008934:Mitogens; D010835:Phytohemagglutinins; D012333:RNA, Messenger