Browsing by Author "Slutsky, Rebecca"
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- ItemAre B cells altered in the decidua of women with preterm or term labor?(2019) Leng, Yaozhu; Romero, Roberto; Xu, Yi; Galaz Alarcón, José; Slutsky, Rebecca; Arenas Hernández, Marcia; García Flores, Valeria; Motomura, Kenichiro; Hassan, Sonia S.; Reboldi, Andrea; Gómez López, Nardhy
- ItemCellular immune responses in amniotic fluid of women with preterm clinical chorioamnionitis(2020) Galaz, Jose; Romero, Roberto; Xu, Yi; Miller, Derek; Slutsky, Rebecca; Levenson, Dustyn; Hsu, Chaur-Dong; Gomez-Lopez, NardhyObjective Preterm birth is the leading cause of neonatal morbidity and mortality worldwide. Some preterm births are associated with clinical chorioamnionitis; yet, this condition has been poorly investigated. Herein, we characterized the amniotic fluid cellular immune responses in women with preterm clinical chorioamnionitis. Methods and subjects Amniotic fluid samples were obtained from women with preterm clinical chorioamnionitis and a positive or negative microbiological culture (n = 17). The cellular composition of amniotic fluid was evaluated using fluorescence microscopy, scanning and transmission electron microscopy, and flow cytometry. Women without preterm clinical chorioamnionitis were also examined (n = 10). Results Amniotic fluid from women with preterm clinical chorioamnionitis and a positive culture had: (1) abundant neutrophils associated with viable and non-viable bacteria, (2) neutrophils performing phagocytosis, (3) neutrophils forming NETs, (4) increased numbers of neutrophils, monocytes/macrophages, and CD4+ T cells, and (5) high expression of IL-1 beta by neutrophils and monocytes/macrophages. Amniotic fluid from women with preterm clinical chorioamnionitis and proven infection tended to have fewer monocytes/macrophages and CD4+ T cells compared to those without chorioamnionitis. Conclusion We provide the first morphologic and phenotypic characterization of the cellular immune responses in the amniotic cavity of women with preterm clinical chorioamnionitis, a condition associated with adverse neonatal outcomes.
- ItemCellular immune responses in amniotic fluid of women with preterm prelabor rupture of membranes(WALTER DE GRUYTER GMBH, 2020) Galaz, Jose; Romero, Roberto; Slutsky, Rebecca; Xu, Yi; Motomura, Kenichiro; Para, Robert; Pacora, Percy; Panaitescu, Bogdan; Hsu, Chaur Dong; Kacerovsky, Marian; Gomez Lopez, NardhyBackground: Preterm birth is the leading cause of perinatal morbidity and mortality. Preterm prelabor rupture of membranes (pPROM) occurs in 30% of preterm births; thus, this complication is a major contributor to maternal and neonatal morbidity. However, the cellular immune responses in amniotic fluid of women with pPROM have not been investigated.
- ItemExhausted and Senescent T Cells at the Maternal-Fetal Interface in Preterm and Term Labor(2019) Slutsky, Rebecca; Romero, Roberto; Xu, Yi; Galaz, Jose; Miller, Derek; Done, Bogdan; Tarca, Adi L.; Gregor, Sabrina; Hassan, Sonia S.; Leng, Yaozhu; Gomez-Lopez, NardhySuccessful pregnancy requires a tightly-regulated equilibrium of immune cell interactions at the maternal-fetal interface (i.e., the decidual tissues), which plays a central role in the inflammatory process of labor. Most of the innate immune cells in this compartment have been well characterized; however, adaptive immune cells are still under investigation. Herein, we performed immunophenotyping of the decidua basalis and decidua parietalis to determine whether exhausted and senescent T cells are present at the maternal-fetal interface and whether the presence of pathological (i.e., preterm) or physiological (i.e., term) labor and/or placental inflammation alter such adaptive immune cells. In addition, decidual exhausted T cells were sorted to test their functional status. We found that (1) exhausted and senescent T cells were present at the maternal-fetal interface and predominantly expressed an effector memory phenotype, (2) exhausted CD4(+) T cells increased in the decidua parietalis as gestational age progressed, (3) exhausted CD4(+) and CD8(+) T cells decreased in the decidua basalis of women who underwent labor at term compared to those without labor, (4) exhausted CD4(+) T cells declined with the presence of placental inflammation in the decidua basalis of women with preterm labor, (5) exhausted CD8(+) T cells decreased with the presence of placental inflammation in the decidua basalis of women who underwent labor at term, (6) both senescent CD4(+) and CD8(+) T cells declined with the presence of placental inflammation in the decidua basalis of women who underwent preterm labor, and (7) decidual exhausted T cells produced IFN and TNF upon in vitro stimulation. Collectively, these findings indicate that exhausted and senescent T cells are present at the human maternal-fetal interface and undergo alterations in a subset of women either with labor at term or preterm labor and placental inflammation. Importantly, decidual T cell function can be restored upon stimulation.
- ItemMicrobial burden and inflammasome activation in amniotic fluid of patients with preterm prelabor rupture of membranes(2020) Theis, Kevin R.; Romero, Roberto; Motomura, Kenichiro; Galaz, Jose; Winters, Andrew D.; Pacora, Percy; Miller, Derek; Slutsky, Rebecca; Florova, Violetta; Levenson, Dustyn; Para, Robert; Varrey, Aneesha; Kacerovsky, Marian; Hsu, Chaur-Dong; Gomez-Lopez, NardhyBackground: Intra-amniotic inflammation, which is associated with adverse pregnancy outcomes, can occur in the presence or absence of detectable microorganisms, and involves activation of the inflammasome. lntra-amniotic inflammasome activation has been reported in clinical chorioamnionitis at term and preterm labor with intact membranes, but it has not yet been investigated in women with preterm prelabor rupture of membranes (preterm PROM) in the presence/absence of detectable microorganisms. The aim of this study was to determine whether, among women with preterm PROM, there is an association between detectable microorganisms in amniotic fluid and intra-amniotic inflammation, and whether intra-amniotic inflammasome activation correlates with microbial burden.