Comparative Analysis of Preterm and Full-term Births using Transcriptomic Profiling

<p dir="ltr">Preterm birth (PTB) or delivery prior to 37 weeks of gestation—is one of the most common causes of neonatal morbidity and mortality across the globe. It has been linked to negative health effects including chronic conditions, respiratory distress syndrome, and neurodevel...

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Main Author: Amal E. I. Ahmed (22789562) (author)
Other Authors: Faisal E. Ibrahim (19962788) (author), Bala Subramani Gattu Linga (23752902) (author), Ahmad M. Alqudah (9934071) (author), Nader Al-Dewik (4166527) (author)
Published: 2025
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Summary:<p dir="ltr">Preterm birth (PTB) or delivery prior to 37 weeks of gestation—is one of the most common causes of neonatal morbidity and mortality across the globe. It has been linked to negative health effects including chronic conditions, respiratory distress syndrome, and neurodevelopmental delays. While pre-term labor has clinical importance, its molecular mechanisms are still not fully elucidated. We analysed RNA sequencing (RNA-Seq) data from placenta and maternal whole blood samples obtained from the Gene Expression Omnibus (GEO) to identify differentially expressed genes (DEGs) associated with preterm delivery, with a specific focus on inflammation, hormonal control, and birthing mechanisms. In the placenta, we observed that genes involved with immunological tolerance and endocrine signaling were downregulated. Preterm samples such as <i>CXCL14</i> (chemokine ligand 14) and <i>HSD11B2 </i>(hydroxysteroid 11-beta dehydrogenase 2)were associated with glucocorticoid metabolism and immune modulation dysfunction.</p><p dir="ltr">Furthermore, the exacerbated milieu pointed toward intra-amniotic infection was often accompanied by marked elevation of pro-inflammatory genes such as <i>IL1B</i> (interleukin 1 beta)and <i>PTGS2</i> (prostaglandin-endoperoxide synthase 2). A whole blood maternal assessment showed there was systemic inflammation through upregulation of several genes in preterm cases relative to full terms. <i>IL6</i> (interleukin 6), <i>TNF</i> (tumor necrosis factor), and <i>CXCL8</i> (also known as <i>IL8</i>). On the other hand, homeostatic regulators <i>IL10</i> (interleukin 10)and <i>TGFBR2</i> (transforming growth factor beta receptor 2) demonstrated down regulation portraying an imbalance of immune homeostasis. The placental villous tissue from the preterm birth caused by infection exhibited distinct gene profiles including up-regulation of <i>S100A9</i> and <i>MMP9</i> which are known for neutrophil activation and <i>ECM</i> remodelling. </p><p dir="ltr">Other Inflammation associated processes with positive enrichment include signaling pathways such as NF-κB and <i>TLR</i>. Our findings highlight the complex interplay of genetic and non-genetic factors in preterm labor, the etiology of which remains elusive along with tissue-specific transcriptomic signatures. These results will facilitate the design of sensitive diagnostic tests and tailored treatments which could improve maternal and fetal health outcomes and change approach to clinical management.</p><h2 dir="ltr">Other Information</h2><p dir="ltr">Conference information: 18th Edition of the Qatar University Life Sciences Symposium Bio-Environment: Advances and Innovations. (26 - 27 Nov 2025, Qatar University, Doha - Qatar)<br>License: <a href="https://creativecommons.org/licenses/by/4.0/" rel="noreferrer noopener" target="_blank">https://creativecommons.org/licenses/by/4.0/</a></p><p dir="ltr">See the conference information on the organizer's website: <a href="https://www.qu.edu.qa/en-us/conference/QULSS2025/Pages/default.aspx" rel="noreferrer noopener" target="_blank">https://www.qu.edu.qa/en-us/conference/QULSS2025/Pages/default.aspx</a></p>