Expression of dNK cells and their cytokines in twin pregnancies with preeclampsia
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Citações na Scopus
3
Tipo de produção
article
Data de publicação
2019
Título da Revista
ISSN da Revista
Título do Volume
Editora
HOSPITAL CLINICAS, UNIV SAO PAULO
Citação
CLINICS, v.74, article ID e1200, 5p, 2019
Resumo
OBJECTIVES: To assess the expression of decidual natural killer (dNK) cells and their cytokines in twin pregnancies with preeclampsia. METHODS: This was a prospective case-control study. The inclusion criteria were diamniotic (monochorionic or dichorionic) twin pregnancies in the third trimester with negative serological results for infectious diseases; absence of major fetal abnormalities or twin-twin transfusion syndrome; and no history of administration of corticosteroids in this pregnancy. The control group (CG) included uncomplicated twin pregnancies, and the preeclampsia group (PEG) included twin gestations with clinical and laboratory confirmation of the disease according to well-established criteria. Samples of the decidua were obtained and analyzed by immunohistochemistry for the expression of dNK cells and interleukins (ILs) 10, 12 and 15. In addition, maternal serum samples were collected to determine the levels of these interleukins. RESULTS: Thirty twin pregnancies were selected: 20 in the control group (CG) and 10 in the preeclampsia group (PEG). The PEG showed strong placental immunostaining for IL-15 (p=0.001) and high maternal serum levels of IL-10 (22.7 vs. 11.9 pg/mL, p=0.024) and IL-15 (15.9 vs. 7.4 pg/mL, p=0.024). CONCLUSION: A higher maternal serum concentration of both pro- and anti-inflammatory factors was observed in the twin pregnancies in the PEG. However, no difference in placental expression of IL-10 was found between the groups. These findings may suggest that maternal attempts to balance these interleukins were not sufficient to cause a placental response, and this failure may contribute to the development of preeclampsia.
Palavras-chave
Twin Pregnancy, Preeclampsia, Decidual Natural Killer Cells, Interleukins
Referências
- Amaral LM, 2017, CURR HYPERTENS REP, V19, DOI 10.1007/s11906-017-0757-7
- [Anonymous], 2019, Obstet Gynecol, V133, pe1, DOI 10.1097/AOG.0000000000003018
- Bachmayer N, 2006, AM J REPROD IMMUNOL, V56, P292, DOI 10.1111/j.1600-0897.2006.00429.x
- Cheng SB, 2015, AM J REPROD IMMUNOL, V73, P487, DOI 10.1111/aji.12329
- Cornelius DC, 2018, CLIN MED INSIGHTS-BL, V11, DOI 10.1177/1179545X17752325
- Duley L, 2009, SEMIN PERINATOL, V33, P130, DOI 10.1053/j.semperi.2009.02.010
- Eide IP, 2006, VIRCHOWS ARCH, V448, P269, DOI 10.1007/s00428-005-0107-z
- El-Baradie SMY, 2009, J OBSTET GYNAECOL CA, V31, P142, DOI 10.1016/S1701-2163(16)34098-1
- Faas MM, 2017, PLACENTA, V56, P44, DOI 10.1016/j.placenta.2017.03.001
- Gilbert JS, 2008, AM J PHYSIOL-HEART C, V294, pH541, DOI 10.1152/ajpheart.01113.2007
- Harmon AC, 2016, CLIN SCI, V130, P409, DOI 10.1042/CS20150702
- Hennessy A, 1999, J IMMUNOL, V163, P3491
- Hromadnikova I, 2016, PLOS ONE, V11, DOI 10.1371/journal.pone.0151535
- Kalkunte S, 2011, J REPROD IMMUNOL, V88, P165, DOI 10.1016/j.jri.2011.01.009
- KOBAYASHI M, 1989, J EXP MED, V170, P827, DOI 10.1084/jem.170.3.827
- Madazli R, 2003, ACTA OBSTET GYN SCAN, V82, P797, DOI 10.1034/j.1600-0412.2003.00206.x
- Murphy SP, 2009, BIOL REPROD, V80, P848, DOI 10.1095/biolreprod.108.073353
- Neres R, 2008, PLOS ONE, V3, DOI 10.1371/journal.pone.0001608
- Olusi SO, 2000, ANN SAUDI MED, V20, P4, DOI 10.5144/0256-4947.2000.4
- Pinheiro MB, 2013, CYTOKINE, V62, P165, DOI 10.1016/j.cyto.2013.02.027
- Rieger L, 2009, REPROD BIOL ENDOCRIN, V7, DOI 10.1186/1477-7827-7-132
- Sibai BM, 2000, AM J OBSTET GYNECOL, V182, P938, DOI 10.1016/S0002-9378(00)70350-4
- Sones JL, 2014, AM J PHYSIOL-REG I, V307, pR490, DOI 10.1152/ajpregu.00176.2014
- Stallmach T, 1999, VIRCHOWS ARCH, V434, P207, DOI 10.1007/s004280050329
- Wilczynski JR, 2002, MEDIAT INFLAMM, V11, P105, DOI 10.1080/09629350220131962
- Williams PJ, 2009, REPRODUCTION, V138, P177, DOI 10.1530/REP-09-0007