TY - JOUR
T1 - Patterns of peripheral cytokine expression during pregnancy in two cohorts and associations with inflammatory markers in cord blood
AU - Ross, Kharah Mac Kenzie
AU - Miller, Gregory
AU - Culhane, Jennifer
AU - Grobman, William
AU - Simhan, Hyagriv N.
AU - Wadhwa, Pathik D.
AU - Williamson, Douglas
AU - McDade, Thomas
AU - Buss, Claudia
AU - Entringer, Sonja
AU - Adam, Emma
AU - Qadir, Sameen
AU - Keenan-Devlin, Lauren
AU - Leigh, Adam K.K.
AU - Borders, Ann
N1 - Publisher Copyright:
© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
PY - 2016/11/1
Y1 - 2016/11/1
N2 - Problem: Maternal inflammation undergoes adaptations during pregnancy, and excessive inflammation has been associated with adverse outcomes. One mechanism may be maternal inflammation transmission to the fetal compartment. Links between maternal pregnancy inflammation and fetal inflammation are poorly characterized. Method: Principal components analysis was used to extract underlying inflammation components across cytokines (IFN-γ, IL-10, IL-13, IL-6, IL-8, TNF-α) in two pregnancy cohorts (SPAH N=87, MOMS N=539) assessed during the second and third trimesters. Links between maternal inflammation over pregnancy and fetal (cord blood) inflammation were assessed. Results: Substantial cytokine rank-order stability was observed in both cohorts, β's range.47-.96, P's <.001. Two consistent inflammatory components were extracted: a pro-inflammatory (IL-10, IL-6, IL-8, TNF-α, IFN-γ) component and anti-inflammatory (IL-13) component. Higher maternal pro-inflammatory and lower anti-inflammatory indices during pregnancy were associated with higher cord blood inflammation, P's>.04. Conclusion: Maternal inflammation indices over pregnancy were associated with inflammation in cord blood at birth. Results have implications for understanding pregnancy inflammatory processes and how maternal inflammation may be transmitted to fetal circulation.
AB - Problem: Maternal inflammation undergoes adaptations during pregnancy, and excessive inflammation has been associated with adverse outcomes. One mechanism may be maternal inflammation transmission to the fetal compartment. Links between maternal pregnancy inflammation and fetal inflammation are poorly characterized. Method: Principal components analysis was used to extract underlying inflammation components across cytokines (IFN-γ, IL-10, IL-13, IL-6, IL-8, TNF-α) in two pregnancy cohorts (SPAH N=87, MOMS N=539) assessed during the second and third trimesters. Links between maternal inflammation over pregnancy and fetal (cord blood) inflammation were assessed. Results: Substantial cytokine rank-order stability was observed in both cohorts, β's range.47-.96, P's <.001. Two consistent inflammatory components were extracted: a pro-inflammatory (IL-10, IL-6, IL-8, TNF-α, IFN-γ) component and anti-inflammatory (IL-13) component. Higher maternal pro-inflammatory and lower anti-inflammatory indices during pregnancy were associated with higher cord blood inflammation, P's>.04. Conclusion: Maternal inflammation indices over pregnancy were associated with inflammation in cord blood at birth. Results have implications for understanding pregnancy inflammatory processes and how maternal inflammation may be transmitted to fetal circulation.
KW - cord blood
KW - inflammation
KW - pregnancy
UR - http://www.scopus.com/inward/record.url?scp=84990232766&partnerID=8YFLogxK
U2 - 10.1111/aji.12563
DO - 10.1111/aji.12563
M3 - Journal Article
C2 - 27615067
AN - SCOPUS:84990232766
SN - 1046-7408
VL - 76
SP - 406
EP - 414
JO - American Journal of Reproductive Immunology
JF - American Journal of Reproductive Immunology
IS - 5
ER -