INFLAMMATORY CYTOKINE (INTERLEUKIN-1, INTERLEUKIN-6, AND INTERLEUKIN-8 AND TUMOR-NECROSIS-FACTOR-ALPHA) RELEASE FROM CULTURED HUMAN FETAL MEMBRANES IN RESPONSE TO ENDOTOXIC LIPOPOLYSACCHARIDE MIRRORS AMNIOTIC-FLUID CONCENTRATIONS
Sj. Fortunato et al., INFLAMMATORY CYTOKINE (INTERLEUKIN-1, INTERLEUKIN-6, AND INTERLEUKIN-8 AND TUMOR-NECROSIS-FACTOR-ALPHA) RELEASE FROM CULTURED HUMAN FETAL MEMBRANES IN RESPONSE TO ENDOTOXIC LIPOPOLYSACCHARIDE MIRRORS AMNIOTIC-FLUID CONCENTRATIONS, American journal of obstetrics and gynecology, 174(6), 1996, pp. 1855-1860
OBJECTIVE: This study was conducted to quantitate and compare the amou
nt of cytokines released from human fetal membranes in response to tre
atment with bacterial lipopolysaccharide and to compare this with amni
otic fluid levels. STUDY DESIGN: Amniochorionic membranes were collect
ed from women undergoing elective repeat cesarean section and showing
no signs of infection- or pregnancy-related complications. Membranes w
ere maintained in an organ explant system and stimulated with bacteria
l lipopolysaccharide for 24 hours. Media samples were collected and st
ored at -20 degrees C until cytokine levels were assayed by enzyme-lin
ked immunosorbent assay. RESULTS: Enzyme-linked immunosorbent assay re
sults demonstrated that lipopolysaccharide stimulated production of in
terleukins 1, 6, and 8 and tumor necrosis factor-alpha by the fetal me
mbranes in comparison with the control cultures. A greater release of
interleukin-6 and interleukin-8 compared with interleukin-1 and tumor
necrosis factor-alpha was noticed. The relationships between cytokine
concentrations observed in culture mirror those seen in amniotic fluid
. CONCLUSION: Amniochorionic membranes can respond to an infectious pr
ocess with increased secretion of interleukins 1, 6, and 8 and tumor n
ecrosis factor-alpha. Cytokines produced from both amnion and chorion
(interleukin-6 and interleukin-8) are released in greater quantities t
han those cytokines produced from chorion or amnion alone (interleukin
-1 and tumor necrosis factor-alpha). These studies support a major rol
e for amnion in infection-induced preterm labor.