Secretions of Interleukin-1β and Tumor Necrosis Factor α by Whole Fetal Membranes Depend on Initial Interactions of Amnion or Choriodecidua with Lipopolysaccharides or Group B Streptococci1

Abstract

The present study evaluated the secretions of interleukin (IL)-1beta and tumor necrosis factor (TNF) alpha by fetal membranes stimulated with group B streptococci (GBS) and lipopolysaccharide (LPS). The aim was to evaluate the initial response of full-thickness membranes to the microbial insult using an in vitro experimental model that allowed testing of the individual contributions of amnion and choriodecidua to stimulation. Full-thickness membranes were obtained after delivery by elective cesarean section from women at 37-40 wk of gestation without evidence of active labor. The membranes were mounted in Transwell devices, physically separating the upper and lower chambers. The LPS (500 ng/ml) or GBS (1 x 10(6) colony-forming units/ml) was added to either the amniotic or choriodecidual surface, and accumulation of IL-1beta and TNFalpha were measured in both compartments using a specific ELISA. Fetal membranes followed different patterns of secretion of proinflammatory cytokines that depended on the side to which the stimulus was added or the nature of the stimulus itself. The TNFalpha was secreted by amnion and choriodecidua in the presence of LPS or GBS, and stimulation with GBS induced a greater synthesis of IL-1beta than did stimulation with LPS. Choriodecidual tissue was more responsive than amniotic tissue, and this response tended to be higher even when the stimulation was only on the amniotic side. However, the amnion plays an active role in recognizing LPS or GBS, contributing a significant amount of TNFalpha. Thus, cooperative and bidirectional communications occur between amnion and choriodecidua in response to bacterial products, which include intermembranous cytokine traffic and signaling between tissues.

Tumor Necrosis Factor-α and Interleukin-1β Regulate Interleukin-8 Expression in Third Trimester Decidual Cells

“…The choriodecidua proved more responsive than the amnion. 35 Observations that LPS targets decidual cells and decidual macrophages to secrete TNF-␣ and IL-1␤ 33,[35][36][37] constitute the initial steps of the scheme of infectioninduced PPROM depicted in Figure 8. The current study provides the next step in the proposed scheme by demonstrating that both cytokines enhance IL-8 expression in term decidual cells.…”

Weakening and Rupture of Human Fetal Membranes – Biochemistry and Biomechanics

“…In contrast, both active and latent forms of Bryant-Greenwood et al, 1995;Osmers et al, 1995;Athayde et al, 1999;Vadillo-Ortega et al, 2002). MMP-9 can also be induced in FM tissue with PGE 2 , PGF 2 , TNF and ROS (Buhimschi et al, 2000;Ulug et al, 2001;Arechavaleta-Velasco et al, 2002;Zaga et al, 2004). TIMP-1, which controls the activity of MMP-9, has been extensively studied in FM and found to decrease with PROM and labor (Ulug et al, 2001;Arechavaleta-Velasco et al, 2002;Buhimschi et al, 2000;Zaga et al, 2004;McLaren et al, 2000b).…”

“…MMP-9 can also be induced in FM tissue with PGE 2 , PGF 2 , TNF and ROS (Buhimschi et al, 2000;Ulug et al, 2001;Arechavaleta-Velasco et al, 2002;Zaga et al, 2004). TIMP-1, which controls the activity of MMP-9, has been extensively studied in FM and found to decrease with PROM and labor (Ulug et al, 2001;Arechavaleta-Velasco et al, 2002;Buhimschi et al, 2000;Zaga et al, 2004;McLaren et al, 2000b). Thus we conclude that MMP-9 plays a major role in FM remodeling, weakening and rupture.…”

“…Most of these "apoptotic" agents also increase transcription or activation of MMPs, especially MMP-9 ; R.M. Moore et al, 2009b;Menon et al, 2004;Zaga et al, 2004). Several groups have proposed the synergistic effects of MMP activation and apoptosis leading to rupture of the FM (McLaren et al, 2000a;Fortunato et al, 2000;Bowen et al, 2002;Lei et al, 1996).…”

Role of Nuclear Receptors Peroxisome Proliferator-Activated Receptors (PPARs) and Liver X Receptors (LXRs) in the Human Placental Pathophysiology

“…These ruptures of membranes seem to arise from deregulated proinflammatory factor synthesis. It has already been reported in this pathology that IL1 , IL6, IL8, TNF-, and prostaglandinE(2) show inadequate concentrations in placental membrane and in amniotic fluid (Willi et al, 2002;Zaga et al, 2004;Jacobsson et al, 2005;Zaga-Clavellina et al, 2006). As PPARs may be involved in the occurrence and control of this inflammatory response, further studies are needed to assess their importance in this process and to find new possible therapeutic strategies to prevent this damaging pathology.…”