[Serum concentration of soluble vascular-cellular adhesion molecule-1 (VCAM-1) and expression of its receptor VLA-4 on the surface of peripheral blood and decidual lymphocytes of preeclamptic women].
BACKGROUND
Vascular-cellular adhesion molecule-1 (VCAM-1) overexpression on the cells' surface is stimulated by pro-inflammatory cytokines, bacterial endotoxins, reactive oxygen species and lipid peroxides. In the serum also the soluble form of VCAM-1 (sVCAM-1) is present. The beta 1-integrin family molecule VLA-4 (CD49d) is natural ligand for VCAM-1. Increased concentrations of sVCAM-1 as well as overexpression of VLA-4 were observed during inflammatory reaction.


OBJECTIVE
To study sVCAM-1 serum concentrations and CD49d+ subpopulations of peripheral blood and decidual lymphocytes of the 3rd trimester healthy and preeclamptic women.


METHODS
The study groups: n = 21 healthy pregnant women, n = 33 preeclamptic women (preeclampsia defined as blood pressure > 140/90 mmHg with proteinuria > 0.3 g/24 h). Clinical states of known pathogenesis which could possibly interfere with values of studied parameters were excluded. Exclusion criteria were also uterine contractions and premature rupture of amniotic membranes. Decidua was collected exclusively during elective caesarean sections. The sVCAM-1 concentration (ng/ml) was estimated using ELISA procedure, while percentage (%) of CD49d+ lymphocytes in the whole blood and homogenized decidual tissue, using flow cytometry. The results were presented as median value with 25% and 75% cut off values. Statistical analysis was performed with U-Mann-Whitney test (p < 0.05).


RESULTS
Preeclamptic women presented with increased sVCAM-1 serum concentrations (532.5 (400.0/605.0) ng/ml vs. 387.0 (320.0/416.5) ng/ml, p < 0.0005), increased (%) of CD49d+ peripheral blood (92.0 (88.0/96.0)% vs. 52.9 (47.5/55.8)%, p < 0.0000001) and CD49d+ decidual lymphocytes (88.0 (84.0/90.0)% vs. 80.5 (74.0/85.6)%, p < 0.05).


CONCLUSIONS
Described change suggest that immunological mechanisms similar to inflammatory reaction could be involved in pathogenesis of preeclampsia in peripheral blood as well as locally inside maternal-fetal interface.
Wilczyński
Jacek R
JR
Kliniki Chirurgii Ginekologicznej Instytutu CZMP, Rehabilitacji Ginekologicznej i Połoznictwa Uniwersytetu Medycznego w łodzi.
Głowacka
Ewa
E
Nowak
Marek
M
Szpakowski
Artur
A
D000328:Adult; D016022:Case-Control Studies; D003656:Decidua / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D039441:Integrin alpha4 / Q000097:blood*; D039041:Integrin alpha4beta1 / Q000097:blood*; D008214:Lymphocytes / Q000276:immunology / Q000378:metabolism*; D008431:Maternal-Fetal Exchange; D011225:Pre-Eclampsia / Q000276:immunology*; D011247:Pregnancy; D011263:Pregnancy Trimester, Third; D012016:Reference Values; D018709:Statistics, Nonparametric; D013997:Time Factors; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood*
D039041:Integrin alpha4beta1; D019010:Vascular Cell Adhesion Molecule-1; D039441:Integrin alpha4