scholarly journals OP25.01: Cervical immune response as a predictor of preterm birth

2009 ◽  
Vol 34 (S1) ◽  
pp. 142-143
Author(s):  
T. Stampalija ◽  
M. S. Othman ◽  
J. A. Drury ◽  
L. Heathcot ◽  
S. Quenby ◽  
...  
2021 ◽  
Author(s):  
Gemma Sullivan ◽  
Paola Galdi ◽  
Nis Borbye-Lorenzen ◽  
David Q Stoye ◽  
Gillian J Lamb ◽  
...  

Abstract Objective. To characterise the umbilical cord blood immune profile in preterm infants compared to term-born controls and the postnatal immune response following exposure to histologic chorioamnionitis (HCA) in preterm infants. Design. Descriptive, observational cohort study. Setting. Edinburgh, UK. Population. 118 preterm infants (mean gestational age 29+0 weeks, range 23+2 to 32+0) and 59 term-born controls. Methods. Placental histopathology was used to identify reaction patterns indicative of HCA, and a customised immunoassay of 24 inflammatory markers and trophic proteins selected to reflect the perinatal immune response was performed on umbilical cord blood in term and preterm participants and postnatal day 5 blood in the preterm group. Results. The umbilical cord blood immune profile classified gestational age category with 86% accuracy (95% CI 0.78-0.92), p-value=1.242x10-14. Pro-inflammatory proteins IL-6, MCP-1 and CRP were elevated in the cord blood of preterm infants whilst BDNF, C3, C9, IL-18, MMP-9 and RANTES were decreased, compared to infants born at term. In preterm infants, exposure to HCA was associated with elevations in 5 immune proteins on postnatal day 5 (BDNF, C3, IL-8, MIP-1β and MMP-9) when compared to preterm infants who were not exposed. Conclusion. Preterm birth is associated with a distinct immune profile in umbilical cord blood and infants exposed to HCA experience specific alterations in immune function that persist to day 5 of postnatal life.


2005 ◽  
Vol 193 (3) ◽  
pp. 1121-1126 ◽  
Author(s):  
Kim A. Boggess ◽  
Kevin Moss ◽  
Phoebus Madianos ◽  
Amy P. Murtha ◽  
James Beck ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Gemma Sullivan ◽  
Paola Galdi ◽  
Nis Borbye-Lorenzen ◽  
David Q. Stoye ◽  
Gillian J. Lamb ◽  
...  

IntroductionPreterm infants are at increased risk of exposure to histologic chorioamnionitis (HCA) when compared to term-born controls, and this is associated with several neonatal morbidities involving brain, lungs and gut. Preterm infants could benefit from immunomodulatory therapies in the perinatal period, but development of rational treatment strategies requires improved characterization of the perinatal response to HCA. We had two objectives: The first, to characterize the umbilical cord blood immune profile in preterm infants compared to term-born controls; the second, to investigate the postnatal immune response in preterm infants exposed to HCA versus those who were not.PopulationFor objective one 59 term infants [mean gestational age (GA) 39+4 (37+3 to 42+0)] and 55 preterm infants [mean GA29+0(23+3 to 32+0)] with umbilical cord samples available were included; for objective two we studied 96 preterm infants [mean GA29+1(23+2 to 32+0)] for whom placental histology and postnatal blood samples were available.MethodsPlacental histopathology was used to identify reaction patterns indicative of HCA, and a customized immunoassay of 24 inflammatory markers and trophic proteins selected to reflect the perinatal immune response was performed on umbilical cord blood in term and preterm participants and postnatal day 5 blood in the preterm group.ResultsThe umbilical cord blood immune profile classified gestational age category with 86% accuracy (95% CI 0.78-0.92), p-value=1.242x10-14. Pro-inflammatory proteins IL-6, MCP-1 and CRP were elevated in the cord blood of preterm infants whilst BDNF, C3, C9, IL-18, MMP-9 and RANTES were decreased, compared to infants born at term. In preterm infants, exposure to HCA was associated with elevations in 8 immune proteins on postnatal day 5 (BDNF, C3, C5a, C9, IL-8, MCP-1, MIP-1β and MMP-9) when compared to preterm infants who were not exposed.ConclusionPreterm birth is associated with a distinct immune profile in umbilical cord blood and preterm infants exposed to HCA with evidence of a fetal inflammatory response have specific alterations in immune function that are apparent on day 5 of postnatal life.


2008 ◽  
Vol 199 (6) ◽  
pp. S27
Author(s):  
Brianna Lyttle ◽  
Juan Gonzalez ◽  
Hua Xu ◽  
Ella Ofori ◽  
Michal Elovitz

2009 ◽  
Vol 201 (3) ◽  
pp. 284.e1-284.e7 ◽  
Author(s):  
Brianna Lyttle ◽  
Jinghua Chai ◽  
Juan M. Gonzalez ◽  
Hua Xu ◽  
Mary Sammel ◽  
...  

2016 ◽  
Vol 8 (4) ◽  
pp. 386-399 ◽  
Author(s):  
Sarah McKenna ◽  
Molly Eckman ◽  
Andrew Parker ◽  
Rachael Bok ◽  
K. Joseph Hurt ◽  
...  

Background: Exposure to perinatal infection is associated with the multiple morbidities complicating preterm birth. How a relatively immature innate immune response contributes to this is unknown. Objective: We sought to determine if the perinatal innate immune response to endotoxemia induces a unique pattern of cyclooxygenase-2 (COX-2) expression via an NFκB-dependent mechanism. Methods: Hepatic and pulmonary COX-2 mRNA expression was assessed following perinatal (at embryonic days 15 and 19 and after birth) or adult endotoxemia. Hepatic NFκB activity was assessed by cytosolic inhibitory protein degradation and subunit nuclear translocation. Immunohistochemistry and isolated cell preparations determined hepatic macrophage COX-2 expression, and the effect of pharmacologic and genetic inhibition of NFκB activity was tested. Results: Perinatal endotoxemia induced sustained hepatic macrophage COX-2 expression and NFκB activity compared to in exposed adults. Isolated hepatic macrophages and immunohistochemistry demonstrated enriched LPS-induced COX-2 expression that was sensitive to pharmacologic and genetic approaches to attenuate NFκB activity. Finally, pharmacologic inhibition of endotoxemia-induced NFκB activity in neonatal mice prevented hepatic NFκB activity and attenuated COX-2 expression. Conclusion: Our findings of sustained neonatal hepatic NFκB activity and COX-2 expression in response to endotoxemia support a robust perinatal innate immune response. This may represent a link between the innate immune response and the pathogenesis of diseases associated with preterm birth.


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