Stress increases VCAM-1 expression at the fetomaternal interface in an abortion prone mouse model

PRADOS MB; SOLANO ME; FRIEBE A; BLOIS S; ARCK P; MIRANDA S

CABA

Congreso; First French-Argentine Immunology Congress; 2010

SAI-Grupo Rioplatense de Citometria de Flujo-SAP (Inmunología pediátrica)

Numerous mechanisms involved in abortion processes have been described locally at the fetomaternal interface and systemically, largely arising from studies employing the high fetal loss mouse model (CBA/JxDBA/2J, H2kxH2d). A 24 hs sound stress at 5.5 gestation day (gd) increased the fetal resorption rate (FRR) of DBA/2J mated CBA/J mice but not of BALB/C mated CBA/J females (low fetal loss model, H2kxH2d). Sound stress increases fetal loss via inflammatory pathways. Inflammation up-regulates cell adhesion molecules, which induce cell recruitment to the site of inflammation. In this context, vascular cell adhesion molecule-1 (VCAM-1) mediates the adhesion of leukocytes to vascular endothelium after the endothelial cells have been stimulated by cytokines like TNF-a. Thus, in the present work, we aimed to study the frequency of VCAM-1+ vessels at fetomaternal interface in stressed and non-stressed pregnant CBA/J female mice mated with DBA/2J or BALB/C males. Pregnant females were divided into control group and stressed group.  The latter were exposed to sound stress. Both groups were sacrificed on gd 6.5 and implantation units were removed and cryo-sectioned. The number of vessels per tissue section was determined by PECAM immunostaining. Vessels were classified into small, medium and large according to its size. VCAM-1 expression was analyzed by immunohistochemistry in the cryosections. We observed that both stressed groups had similar number of large vessels. However, stress duplicated the number of large vessels expressing VCAM-1 in the high fetal loss model (p<0.01), whereas a not significant increase of VCAM-1 expression was detected in the low fetal loss model. We propose that up-regulation of VCAM-1 at the fetomaternal interface in abortion prone mice contributes to the perpetuation of decidual inflammation, subsequently leading to placental damage and increased fetal loss.