Placental immunopathology in the FIV-infected cat: a role for inflammation in compromised pregnancy?
In utero transmission of feline immunodeficiency virus (FIV) occurs frequently in queens experimentally infected with FIV-B-2542 and other FIV isolates. Fetal infection has been detected as early as 3-4 weeks gestation, and the incidence of fetal infection increases with progressing gestation. Reproductive failure occurs commonly, including fetal resorptions and developmentally-arrested fetuses, demonstrating that fetal demise occurs early in gestation. Precise, temporal immunomodulation within the placenta is essential for successful pregnancy. Placental Th1 and Th2 cytokines must be appropriately balanced, typically favoring Th2 cytokines at the maternal-fetal interface. Abnormal inflammatory cytokine expression often accompanies miscarriage. Regulatory T cells (Tregs) play an essential role in maternal tolerance of the semi-allogeneic fetus by suppressing inflammation. We are using the FIV-infected cat to examine the relationship between lentivirus-induced placental immunopathology and reproductive outcome. Using TaqMan real time reverse transcriptase (RT)-PCR, we measured relative expression of key immunomodulators in the placentas of FIV-B-2542-infected and control cats, including placentas from both viable and nonviable pregnancies. Our data associate significantly-increased expression of inflammatory cytokines with failed pregnancies, identify Treg markers in the placentas, and provide preliminary evidence that Tregs or other cells bearing similar activation markers may be involved in pregnancy maintenance. Our data suggest that placental inflammation in the FIV-infected cat may compromise pregnancy.
Coats
Karen S
KS
Department of Biological Sciences, P.O. Box GY, Mississippi State University, Mississippi State, MS 39762, USA. kcoats@biology.msstate.edu
Boudreaux
Crystal E
CE
Clay
Brittany T
BT
Lockett
Nikki N
NN
Scott
Veronica L
VL
D000818:Animals; D002415:Cats / Q000276:immunology / Q000821:virology; D018925:Chemokines / Q000096:biosynthesis; D016207:Cytokines / Q000096:biosynthesis; D016181:Feline Acquired Immunodeficiency Syndrome / Q000276:immunology* / Q000473:pathology / Q000821:virology; D005260:Female; D015658:HIV Infections / Q000276:immunology / Q000821:virology; D006801:Humans; D018445:Infectious Disease Transmission, Vertical / Q000662:veterinary; D016180:Lentivirus Infections / Q000276:immunology / Q000662:veterinary / Q000821:virology; D010920:Placenta / Q000276:immunology* / Q000473:pathology / Q000821:virology; D011247:Pregnancy / Q000276:immunology; D011251:Pregnancy Complications, Infectious / Q000276:immunology / Q000662:veterinary* / Q000821:virology; D011256:Pregnancy Outcome / Q000662:veterinary; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000821:virology
D018925:Chemokines; D016207:Cytokines