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Updated: Aug 4, 2026
In Vitro Culture of Epithelial Cells from Different Anatomical Regions of the Human Amniotic Membrane
Published on: November 28, 2019
Profiling epithelial viral receptor expression in amniotic membrane and nasal epithelial cells at birth
Bailee Renouf1, Erika N Sutanto2, Courtney Kidd3
1Telethon Kids Institute, Wal-yan Respiratory Research Centre, Perth, 6009, Western Australia, Australia; School of Health Sciences, The University of Notre Dame Australia, Fremantle, 6160, Western Australia, Australia.
Insights
The amniotic membrane expresses viral receptors found in newborn airways, suggesting the in utero environment may influence prenatal programming of infant respiratory viral defenses.
Area of Science:
- Obstetrics and Gynecology
- Pediatric Pulmonology
- Virology
Background:
- Infants with wheeze and asthma exhibit airway epithelial vulnerabilities impacting viral infection responses.
- The prenatal environment is a potential contributor to the development of these airway epithelial vulnerabilities.
Purpose of the Study:
- To investigate the expression of viral receptors for rhinovirus (RV), respiratory syncytial virus (RSV), and SARS-CoV-2 in the amniotic membrane.
- To compare the expression pattern of these viral receptors in the amniotic membrane with that of newborn nasal epithelium.
Main Methods:
- Quantitative real-time polymerase chain reaction (qPCR) was used to assess gene expression of viral receptors in amniotic membrane samples (n=33) and newborn nasal epithelial cells (n=20).
- Western blot and immunohistochemical staining were employed to confirm and localize protein expression of these receptors in amniotic samples.
Main Results:
- Viral receptors for RV (ICAM-1, LDLR, CDHR3), RSV (NCL, CX3CR1), and SARS-CoV-2 (ACE2, TMPRSS2) were detected at the gene level in both amniotic and newborn nasal samples, with varying expression magnitudes.
- Protein expression of these viral receptors was confirmed in the amniotic membrane and localized to the epithelial layer.
Conclusions:
- This study demonstrates that amniotic membrane samples can be utilized to study prenatal exposure to viruses.
- Findings suggest the in utero environment may play a role in the prenatal programming of epithelial innate immune responses to viral infections in infants.
Introduction:
Children with wheeze and asthma present with airway epithelial vulnerabilities, such as impaired responses to viral infection. It is postulated that the in utero environment may contribute to the development of airway epithelial vulnerabilities. The aims of the study were to establish whether the receptors for rhinovirus (RV), respiratory syncytial virus (RSV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are expressed in the amniotic membrane and whether the pattern of expression is similar to newborn nasal epithelium.
Methods:
Placenta were collected (n = 33) from newborns in AERIAL, a sub-study nested under the ORIGINS birth cohort. Using purified RNA from amniotic samples (n = 33), along with previously extracted RNA from nasal epithelial cells from newborns (n = 20), real-time quantitative polymerase chain reaction (qPCR) was performed to determine gene expression of viral receptors for RV, RSV and SARS-CoV-2 in both amniotic and newborn nasal epithelial samples. In addition, receptor protein expression was quantified through Western blot and localised using immunohistochemical staining in amniotic samples.
Results:
Amniotic and newborn nasal samples expressed various receptors for RV (ICAM-1, LDLR, CDHR3), RSV (NCL, CX3CR1) and SARS-CoV-2 (ACE2, TMPRSS2) at the gene level, although the magnitude of expression varied. In addition, protein expression of these receptors was confirmed in the amniotic samples. These proteins were localised to the epithelial layer of the amniotic membrane.
Conclusion:
This proof-of-concept study indicates the potential of amniotic samples to facilitate investigation into the interactions between the in utero environment and prenatal programming of epithelial innate immune responses to viruses.
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