Expression of plasma nuclear factor KAPPA-B (NFκB) and inhibitory subunit KAPPA B ALPHA (IκB-α) in HIV-associated pre-eclamsia.

Abstract

Objective: The relationship between pre-eclampsia and HIV-1 infection is one of the most unexplored relationships in research. Pre-eclampsia is characterized by inflammation and HIV is characterized by a decline in immune activity. The NFκB pathway is involved in pre-eclampsia and in HIV-1 infection as a transcriptional factor in both conditions. Previous literature has showed that NFκB is upregulated in both pre-eclampsia and HIV-1 infection. Therefore, the aim of this study was to investigate the level of plasma NFκB and the inhibitory subunit IκB-α in HIV associated pre-eclampsia. Method: This retrospective study examined plasma NFκB and IκB-α expression in normotensive (n =32) and preeclamptic (n = 34) HIV positive and HIV negative pregnant women. Quantification of plasma NFκB and IκB-α expression were done using a Bio-Plex Multiplex immunoassay. Results: Our results demonstrated a significant decrease in the level of plasma NFκB expression in pre-eclamptic compared to normotensive pregnancies (p< 0.05), irrespective of HIV status. However, the level of plasma NFκB expression was not significantly different between HIV positive and HIV negative women, irrespective of pregnancy type. Moreover, a significant difference in NFκB expression across all the study groups was observed, specifically a significant decrease in NFκB expression in HIV positive pre-eclamptic women compared to normotensive women (p < 0.05). Furthermore, based on pregnancy type, a significant decrease in the level of plasma IκB-α expression was noted in pre-eclamptic compared to normotensive pregnancies, irrespective of HIV status (p< 0.05). However, our results showed no significant difference across all groups. Although no significance was xii observed, a downwards trend in plasma IκB-α expression was observed in HIV positive pre-eclamptic compared to normotensive women. Conclusion: Our study demonstrates decreased plasma NFκB and IκB-α expression in preeclamptic women irrespective of HIV status. This could be attributed to oxidative stress as an underlying factor subsequently leading to decreased plasma NFκB and IκB-α in preeclamptic women. HIV status had no effect on Plasma NFκB and IκB-α expression. The similarity in plasma NFκB and IκB-α expression based on HIV status may be due to antiretroviral therapy.