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2. Adoptive transfer of placental ischemia‐stimulated natural killer cells causes a preeclampsia‐like phenotype in pregnant rats

Author

Travis, Olivia K., primary, Baik, Cedar, additional, Tardo, Geilda A., additional, Amaral, Lorena, additional, Jackson, Carmilya, additional, Greer, Mallory, additional, Giachelli, Chelsea, additional, Ibrahim, Tarek, additional, Herrock, Owen T., additional, Williams, Jan M., additional, and Cornelius, Denise C., additional

Published
2020
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13. Adoptive transfer of placental ischemia‐stimulated natural killer cells causes a preeclampsia‐like phenotype in pregnant rats.

Author

Travis, Olivia K., Baik, Cedar, Tardo, Geilda A., Amaral, Lorena, Jackson, Carmilya, Greer, Mallory, Giachelli, Chelsea, Ibrahim, Tarek, Herrock, Owen T., Williams, Jan M., and Cornelius, Denise C.

Subjects
*KILLER cells, *RATS, *FETAL growth retardation, *VASCULAR resistance, *PHENOTYPES
Abstract

Problem: The Reduced Uterine Perfusion Pressure (RUPP) rat model of placental ischemia recapitulates many characteristics of preeclampsia including maternal hypertension, intrauterine growth restriction (IUGR), and increased cytolytic natural killer cells (cNKs). While we have previously shown a 5‐fold higher cytotoxicity of RUPP NKs versus normal pregnant NKs, their role in RUPP pathophysiology remains unclear. In this study, we tested the hypotheses that (1) adoptive transfer of RUPP‐stimulated NKs will induce maternal hypertension and IUGR in normal pregnant control (Sham) rats and (2) adoptive transfer of Sham NKs will attenuate maternal hypertension and IUGR in RUPP rats. Method of Study: On gestation day (GD)14, vehicle or 5 × 106 RUPP NKs were infused i.v. into a subset of Sham rats (Sham+RUPP NK), and vehicle or 5 × 106 Sham NKs were infused i.v. into a subset of RUPP rats (RUPP+Sham NK; n = 12/group). On GD18, Uterine Artery Resistance Index (UARI) was measured. On GD19, mean arterial pressure (MAP) was measured, animals were sacrificed, and blood and tissues were collected for analysis. Results: Adoptive transfer of RUPP NKs into Sham rats resulted in elevated NK activation, UARI, placental oxidative stress, and preproendothelin expression as well as reduced circulating nitrate/nitrite. This led to maternal hypertension and IUGR. RUPP recipients of Sham NKs demonstrated normalized NK activation, sFlt‐1, circulating and placental VEGF, and UARI, which led to improved maternal blood pressure and normal fetal growth. Conclusion: These data suggest a direct role for cNKs in causing preeclampsia pathophysiology and a role for normal NKs to improve maternal outcomes and IUGR during late gestation. [ABSTRACT FROM AUTHOR]

Published
2021
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14. 1816

Author

Borges, Marivee, primary, Tramel, Robert, additional, Travis, Olivia, additional, Baik, Cedar, additional, Greer, Mallory, additional, Lemon, James, additional, Williams, Jan, additional, and Cornelius, Denise, additional

Published
2019
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15. NLRP3 inflammasome activation in platelets in response to sepsis.

Author

Cornelius, Denise C., Baik, Cedar H., Travis, Olivia K., White, Dakota L., Young, Cassandra M., Austin Pierce, W., Shields, Corbin A., Poudel, Bibek, and Williams, Jan M.

Subjects
*BLOOD platelet activation, *SEPSIS, *THERAPEUTICS, *CECUM
Abstract

Sepsis is a complex syndrome characterized by organ dysfunction and a dysregulated immune host response to infection. There is currently no effective treatment for sepsis, but platelets have been proposed as a potential therapeutic target for the treatment of sepsis. We hypothesized that the NLRP3 inflammasome is activated in platelets during sepsis and may be associated with multiorgan injury in response to polymicrobial sepsis. Polymicrobial sepsis was induced by cecal ligation and puncture (CLP) in 12‐ to 13‐week‐old male Sprague–Dawley rats. The necrotic cecum was removed at 24 h post‐CLP. At 72 h post‐CLP, activated platelets were significantly increased in CLP versus Sham rats. Colocalization of NLRP3 inflammasome components was observed in platelets from CLP rats at 72 h post‐CLP. Plasma, pulmonary, and renal levels of IL‐1β and IL‐18 were significantly higher in CLP rats compared to Sham controls. Soluble markers of endothelial permeability were increased in CLP versus Sham. Renal and pulmonary histopathology were markedly elevated in CLP rats compared to Sham controls. NLRP3 is activated in platelets in response to CLP and is associated with inflammation, endothelial permeability and multiorgan injury. Our results indicate that activated platelets may play a role to cause multiorgan injury in sepsis and may have therapeutic potential for the treatment of sepsis multiorgan injury. [ABSTRACT FROM AUTHOR]

Published
2019
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