“…Here, we also found dramatic induction of SAA1 expression by LPS in the placenta. Additionally, pronounced increases in SAA1 levels in the maternal blood in preterm deliveries with infectious histologic chorioamnionitis as revealed in this study as well as in previous studies (30,31) lend further support for the participation of SAA1 in infection-induced inflammation in labor process. What's more, the findings of stimulation of SAA1 expression and secretion by LPS in trophoblasts suggest that fetal placenta may contribute to the SAA1 pool together with maternal liver in the maternal blood in preterm birth with infection.…”
Serum amyloid A1 (SAA1) is an acute phase protein produced mainly by the liver to participate in immunomodulation in both sterile and non-sterile inflammation. However, non-hepatic tissues can also synthesize SAA1. It remains to be determined whether SAA1 synthesized locally in the placenta participates in parturition via eliciting inflammatory reactions. In this study, we investigated this issue by using human placenta and a mouse model. We found that SAA1 mRNA and protein were present in human placental villous trophoblasts, which was increased upon syncytialization as well as treatments with lipopolysaccharides (LPS), tumor necrosis factor-α (TNF-α), and cortisol. Moreover, significant increases in SAA1 abundance were observed in the placental tissue or in the maternal blood in spontaneous deliveries without infection at term and in preterm birth with histological chorioamnionitis. Serum amyloid A1 treatment significantly increased parturition-pertinent inflammatory gene expression including interleukin-1β (IL-1β), IL-8, TNF-α, and cyclooxygenase-2 (COX-2), along with increased PGF2α production in syncytiotrophoblasts. Mouse study showed that SAA1 was present in the placental junctional zone and yolk sac membrane, which was increased following intraperitoneal administration of LPS. Intraperitoneal injection of SAA1 not only induced preterm birth but also increased the abundance of IL-1β, TNF-α, and COX-2 in the mouse placenta. Conclusively, SAA1 can be synthesized in the human placenta, which is increased upon trophoblast syncytialization. Parturition is accompanied with increased SAA1 abundance in the placenta. Serum amyloid A1 may participate in parturition in the presence and absence of infection by inducing the expression of inflammatory genes in the placenta.
“…Here, we also found dramatic induction of SAA1 expression by LPS in the placenta. Additionally, pronounced increases in SAA1 levels in the maternal blood in preterm deliveries with infectious histologic chorioamnionitis as revealed in this study as well as in previous studies (30,31) lend further support for the participation of SAA1 in infection-induced inflammation in labor process. What's more, the findings of stimulation of SAA1 expression and secretion by LPS in trophoblasts suggest that fetal placenta may contribute to the SAA1 pool together with maternal liver in the maternal blood in preterm birth with infection.…”
Serum amyloid A1 (SAA1) is an acute phase protein produced mainly by the liver to participate in immunomodulation in both sterile and non-sterile inflammation. However, non-hepatic tissues can also synthesize SAA1. It remains to be determined whether SAA1 synthesized locally in the placenta participates in parturition via eliciting inflammatory reactions. In this study, we investigated this issue by using human placenta and a mouse model. We found that SAA1 mRNA and protein were present in human placental villous trophoblasts, which was increased upon syncytialization as well as treatments with lipopolysaccharides (LPS), tumor necrosis factor-α (TNF-α), and cortisol. Moreover, significant increases in SAA1 abundance were observed in the placental tissue or in the maternal blood in spontaneous deliveries without infection at term and in preterm birth with histological chorioamnionitis. Serum amyloid A1 treatment significantly increased parturition-pertinent inflammatory gene expression including interleukin-1β (IL-1β), IL-8, TNF-α, and cyclooxygenase-2 (COX-2), along with increased PGF2α production in syncytiotrophoblasts. Mouse study showed that SAA1 was present in the placental junctional zone and yolk sac membrane, which was increased following intraperitoneal administration of LPS. Intraperitoneal injection of SAA1 not only induced preterm birth but also increased the abundance of IL-1β, TNF-α, and COX-2 in the mouse placenta. Conclusively, SAA1 can be synthesized in the human placenta, which is increased upon trophoblast syncytialization. Parturition is accompanied with increased SAA1 abundance in the placenta. Serum amyloid A1 may participate in parturition in the presence and absence of infection by inducing the expression of inflammatory genes in the placenta.
“…The results of the meta-analysis based on the p-value functions of each study are displayed in a drapery plot (p-value on the y-axis and the effect size on the x-axis) (Figure 3). [22][23][24][25][26].…”
Section: Results Of Synthesesmentioning
confidence: 99%
“…The finding of negative correlations between maternal serum amyloid A (mSAA) and gestational age or birth weight was uncommon in the studies included in our review. Only one study conducted by Ibrahim et al [ 23 ] reported significant negative correlations between mSAA levels and both gestational age and birth weight. The correlation coefficient was −0.687 ( p < 0.001) for gestational age at birth and −0.552 ( p < 0.001) for neonatal birth weight.…”
Section: Discussionmentioning
confidence: 99%
“… The effect size and heterogeneity based on omitting different included studies [ 22 , 23 , 24 , 25 , 26 ]. …”
Section: Figurementioning
confidence: 99%
“… Forest plot of the correlation between SAA and preterm birth/PROM [ 22 , 23 , 26 ] after excluding outliners. …”
Background and Objectives: Preterm birth, one of the leading causes of neonatal mortality, occurs in between 5 and 18% of births. Premature birth can be induced by a variety of triggers, including infection or inflammation. Serum amyloid A, a family of apolipoproteins, increases significantly and rapidly at the onset of inflammation. This study aims to systematically review the results of studies in the literature that have examined the correlation between SAA and PTB/PROM. Materials and Methods: To examine the correlation between serum amyloid A levels in women who gave birth prematurely, a systematic analysis was performed according to PRISMA guidelines. Studies were retrieved by searching the electronic databases PubMed and Google Scholar. The primary outcome measure was the standardized mean difference in serum amyloid A level comparing the preterm birth or premature rupture of membranes groups and the term birth group. Results: Based on the inclusion criteria, a total of 5 manuscripts adequately addressed the desired outcome and were thus included in the analysis. All included studies showed a statistically significant difference in serum SAA levels between the preterm birth or preterm rupture of membranes groups and the term birth group. The pooled effect, according to the random effects model, is SMD = 2.70. However, the effect is not significant (p = 0.097). In addition, the analysis reveals an increased heterogeneity with an I2 = 96%. Further, the analysis of the influence on heterogeneity found a study that has a significant influence on heterogeneity. However, even after outline exclusion, heterogeneity remained high I2 = 90.7%. Conclusions: There is an association between increased levels of SAA and preterm birth/PROM, but studies have shown great heterogeneity.
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