Abstract
Amniochorion membranes were collected from 25 pregnant women at preterm labor, in the presence or not of Preterm Premature Rupture of Membranes (PPROM) and 27 pregnant women at term in the presence at labor, in order to quantify the expression and to evaluate the immunoreactivity of human beta defensins (HBD)1, HBD2, HBD3 and HBD4 in amniochorion membranes from pregnancies complicated by spontaneous prematurity. The HBDs were evaluated by immunohistochemistry, real time quantitative PCR and ELISA. Statistical analyses were performed using Chi-squared and Mann Whitney tests. There was no significant difference in HBDs expression between study and control groups: HBD1 (Md = 0.62 (0.0 - 105.0) vs Md = 0.80 (0.02 - 25.0); p = 0.85), HBD2 (Md = 0.17 (0.0 - 5.2) vs Md = 0.0 (0.0 - 43.2); p = 0.16), HBD3 (Md = 0.11 (0.0 - 140.5) vs Md = 0.06 (0.0 - 972.1); p = 0.91). Also, HBD1, HBD2 and HBD3 protein expression was not significant different between the groups: HBD1 (1.32 pg/mL (0.0 - 1.85) vs 1.08 pg/mL (0.04 - 2.22); p = 0.67), HBD2 (0.00 pg/mL (0.0 - 1.74) vs 0.02 pg/mL (0.0 - 1.24); p = 0.69), HBD3 (0.04 pg/mL (0.0 - 1.05) vs 0.09 pg/mL (0.0 - 1.05); p = 0.63). The immunoreactivity of HBD1, HBD2 and HBD3 was observed in amnion, chorion and decidua cells from preterm and term pregnancies. Amniochorion membranes are sources of HBD1, HBD2 and HBD3 and their expressions are similar in term and preterm pregnancies.
Highlights
Preterm birth (PTB) affects 11.1% of all pregnancies worldwide [1], in which 70% are spontaneous [2] and present multifactorial etiology, as infection or inflammation, uteroplacental ischaemia or haemorrhage, uterine overdistension or stress [3] and maternal risk factors as previous PTB [4]
Considering that inflammatory events in the amniotic cavity could be pronounced in the preterm pregnancy and that fetal membranes have inhibitory effect in the bacteria growth, partially, by human beta defensins production, we aimed to quantify the protein and gene expression and to evaluate the immunoreactivity of HBD1, HBD2, HBD3 and HBD4 in amniochorion membranes from pregnancies complicated by spontaneous prematurity
The results obtained in this study showed that human beta defensins levels did not correlate positively with advancing gestation (Figure 1)
Summary
Preterm birth (PTB) affects 11.1% of all pregnancies worldwide [1], in which 70% are spontaneous [2] and present multifactorial etiology, as infection or inflammation, uteroplacental ischaemia or haemorrhage, uterine overdistension or stress [3] and maternal risk factors as previous PTB [4]. The infection of the amniotic cavity triggers the immune response and lead to an inflammation with different production of cytokines and Toll-Like Receptors (TLR) expression modifying the normal scenario of gestation and culminating to the PTB [8]. In the presence of microbial invasion of the amniotic cavity (MIAC) the innate immune response has an important role to eliminate the pathogens and re-establish the normal environment of the amniotic cavity, in this sense, the natural antimicrobial peptides are important since they provide protection against microorganism’s infection [9] [10]. Human beta defensins (HBDs) are important contributors to host immunity [9]. The expression and release these peptides depend on the defensins and cell type and stimuli (cytokines/chemokines and microorganisms) being constitutive or inducible regulated. HBD2 is highly inducible in the presence of IL-1β, IL-8 [15], [16], tumor necrosis factor-alpha (TNF-α), lipopolysaccharide (LPS), gram-negative and gram-positive bacteria and yeast [13] [17] [18] [19] [20], while HBD3 is inducible by TNF-α, heat-inactivated bacteria [21] and interferon-γ [22]
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