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Pre-Eclampsia Comorbid with HIV Infection Mimics the Release of sVCAM-1, sICAM-1, and sE-Selectin in African Women
Samukelisiwe Sibiya1,2, Mbuso H Mthembu2, Shoohana Singh2
1HIV Pathogenesis Programme, Doris Duke Medical Research Institute, College of Health Sciences, University of KwaZulu-Natal, Durban 4041, South Africa.
Insights
This study reveals altered levels of soluble cell adhesion molecules in pregnant women with HIV and pre-eclampsia. These changes in soluble vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), and E-selectin (sE-selectin) highlight potential disease mechanisms.
Area of Science:
- Immunology
- Obstetrics
- Infectious Diseases
Background:
- Endothelial activation and cell adhesion molecules (CAMs) are implicated in the pathophysiology of both HIV infection and pre-eclampsia.
- The interplay between HIV and pre-eclampsia may exacerbate endothelial dysfunction, impacting pregnancy outcomes.
Purpose of the Study:
- To compare plasma concentrations of soluble vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), and E-selectin (sE-selectin) in HIV-infected pregnant women with and without pre-eclampsia.
- To investigate the independent and combined effects of HIV infection and pre-eclampsia on these biomarkers.
Main Methods:
- Plasma concentrations of sVCAM-1, sICAM-1, and sE-selectin were measured using immunoassay in 40 normotensive pregnant women and 40 pre-eclamptic women.
- Participants were stratified based on HIV status (positive vs. negative) and pregnancy status (normotensive vs. pre-eclamptic).
Main Results:
- sVCAM-1 and sE-selectin levels were significantly different in pre-eclamptic versus normotensive groups, irrespective of HIV status.
- sICAM-1 and sE-selectin concentrations were elevated in HIV-positive compared to HIV-negative groups, regardless of pregnancy type.
- Significant differences in sICAM-1, sVCAM-1, and sE-selectin were observed between specific subgroups when considering both HIV status and pre-eclampsia.
Conclusions:
- A dysregulation of sICAM-1, sVCAM-1, and sE-selectin occurs in the co-morbidity of pre-eclampsia in pregnant women living with HIV.
- This differential expression may be linked to oxidative stress and hypoxic endothelial activation, potentially exacerbated by antiretroviral therapy.
Abstract:
Endothelial activation and cell adhesion molecules (CAMs) are exacerbated in the interaction of HIV infection and pre-eclampsia. This study compares the levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1), and E-selectin (sE-selectin) in HIV-infected normotensive pregnant versus pre-eclamptic women. We investigated the plasma concentration of sVCAM-1, sICAM-1, and sE-selectin in normotensive pregnant women (n = 40) and pre-eclamptic women (n = 40) using an immunoassay procedure. The concentrations of both sVCAM-1 (p < 0.0083) and sE-selectin (p < 0.0260) were significantly different from sICAM-1 in pre-eclampsia compared to normotensive pregnant groups, irrespective of HIV status. In contrast to sVCAM-1, sICAM-1 (p = 0.0349) and sE-selectin (p < 0.0445) concentrations were significantly elevated in HIV-positive compared to HIV-negative groups, regardless of pregnancy type. In pregnancies complicated by HIV, statistically significant differences in ICAM-1 concentration were observed between pre-eclamptic HIV-positive versus pre-eclamptic HIV-negative groups (p < 0.0010). Similarly, sVCAM-1 levels differed significantly between pre-eclamptic HIV-negative and normotensive HIV-positive groups (p < 0.0139). In contrast, sE-selectin levels varied significantly between pre-eclamptic HIV-positive versus normotensive HIV-negative groups (p < 0.0485). We report a dysregulation of sICAM-1, sVCAM-1, and SE-selectin in the co-morbidity of pre-eclampsia in pregnant women living with HIV. This differential expression may be attributed to oxidative stress emanating from the hypoxic endothelial activation in both pre-eclampsia and HIV infection and exacerbated by the immune restorative action of antiretroviral therapy.
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