Diagnostics (Apr 2022)

Loss of CXC-Chemokine Receptor 1 Expression in Chorioamnionitis Is Associated with Adverse Perinatal Outcomes

  • Yin Ping Wong,
  • Noorhafizah Wagiman,
  • Jonathan Wei De Tan,
  • Barizah Syahirah Hanim,
  • Muhammad Syamil Hilman Rashidan,
  • Kai Mun Fong,
  • Naufal Naqib Norhazli,
  • Yashini Qrisha,
  • Raja Norazah Raja Alam Shah,
  • Muaatamarulain Mustangin,
  • Haliza Zakaria,
  • Siew Xian Chin,
  • Geok Chin Tan

DOI
https://doi.org/10.3390/diagnostics12040882
Journal volume & issue
Vol. 12, no. 4
p. 882

Abstract

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Background: Chorioamnionitis complicates about 1–5% of deliveries at term and causes about one-third of stillbirths. CXC-chemokine receptor 1 (CXCR1) binds IL-8 with high affinity and regulates neutrophil recruitment. We aimed to determine the immunoexpression of CXCR1 in placentas with chorioamnionitis, and its association with adverse perinatal outcomes. Methods: A total of 101 cases of chorioamnionitis and 32 cases of non-chorioamnionitis were recruited over a period of 2 years. CXCR1 immunohistochemistry was performed, and its immunoexpression in placentas was evaluated. The adverse perinatal outcomes included intrauterine death, poor APGAR score, early neonatal death, and respiratory complications. Results: Seventeen cases (17/101, 16.8%) with chorioamnionitis presented as preterm deliveries. Lung complications were more common in mothers who were >35 years (p = 0.003) and with a higher stage in the foetal inflammatory response (p = 0.03). Notably, 24 cases (23.8%) of histological chorioamnionitis were not detected clinically. Interestingly, the loss of CXCR1 immunoexpression in the umbilical cord endothelial cells (UCECs) was significantly associated with foetal death (p = 0.009). Conclusion: The loss of CXCR1 expression in UCECs was significantly associated with an increased risk of adverse perinatal outcomes and could be used as a biomarker to predict adverse perinatal outcomes in chorioamnionitis. Further study is warranted to study the pathophysiology involved in the failure of CXCR1 expression in these cells.

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