///2014 Abstract Details
2014 Abstract Details2019-07-18T14:34:47-06:00

IL-8 production in lung endothelial cells after exposure to preeclamptic plasma

Abstract Number: F-30
Abstract Type: Original Research

Jennifer M Lucero MD, MA1 ; Kevin Wilhelmsen PhD2; Alphonos Tran BA3; Mandy Bell PhD4; Susan Fisher PhD5; Judith Hellman MD6

Preeclampsia effects 5-7% of the pregnant population (1). Pulmonary edema is one of the most common morbidities in women with Pre-E (2). We hypothesized that factors in the plasma of women with Pre-E modulate endothelial functions, including permeability, inflammation, and increase endothelial cell production of soluble endoglin (sEng).

Methods-We obtained samples from Magee Womens Research Institute. Blood was collected in EDTA tubes of normal preterm women (n=5) and preterm Pre-E (n=5) women. Samples were matched for GA, race, smoking, parity, and BMI. Female cadaveric human lung microvascular cells were used for all experiments. Lung endothelial cells were exposed to 5% plasma and incubated 27 hours. Transendothelial resistance, a surrogate for permeability, was measured repeatedly over time using electric cell-substrate impedance sensing (ECIS). Cytokines (IL-8, IL-6) and sEng were measured in endothelial culture supernatants by ELISA.

Results-IL-8 production was significantly increased in the lung endothelial cell after exposure to Pre-E plasma compared to normal plasma (p< .007). IL-6 levels were similar in both groups. There was no significant difference in sEng production in endothelial cells, but there was a significant increase in sEng in Pre-E plasma (p< .004). Transendothelial resistance was not significantly different between cells treated with normal vs. Pre-E plasmas.

Conclusions-Treatment of endothelial cells with plasma from women with Pre-E results in increased production of IL-8, an inflammatory mediator that induces chemotaxis to promote migration of neutrophils to the site of infection. Endothelial cell production of this cytokine could potentially contribute to the increased endothelial cell permeability and consequently pulmonary edema seen clinically in Pre-E. Although, there was not a significant difference in sEng production in the endothelial cell. Literature supports increased production sEng in placentas of women with Pre-E. Our future studies will explore stimulation of lung endothelial cells with sEng and determine the downstream production of factors in the endothelial cell affecting permeability and vascular tone.

References

1.Wallis AB,et al. Secular trends in the rates of preeclampsia, eclampsia, and gestational hypertension, US, 1987–2004. Am J Hypertens 2008;21:521–6.

2.Tufnell,DJ Outcomes of severe preeclampsia/eclampsia in Yorkshire 1999/2003. BJOG: an Inter J of OB-Gyn July 2005, Vol. 112, pp.875-880



SOAP 2014