Abstract
We investigated the mechanisms by which CD8 + T-cell trafficking in placenta contributes to perinatal brain injury by studying effects of maternal CD8 + T-cell depletion (DEP) in a mouse model of intrauterine inflammation (IUI). Maternal CD8 + T cells were depleted with anti-CD8 + antibodies. IUI was induced with lipopolysaccharide (LPS). DEP was confirmed using flow cytometry. Preterm birth rate was evaluated. Offspring neurologic sequelae were assessed by Nissl staining, immune arrays, confirmatory individual TaqMan ® gene assays, and neurobehavioral tests. DEP did not significantly prevent LPS-induced preterm birth but improved neurobehavioral performance (P <.001) and increased cortical neuronal density (P <.05) in LPS-exposed pups compared to controls. These changes were associated with decreased CCL3 and CXCL10 and increased CCL5 in DEP LPS-exposed mice. We demonstrate that DEP reduces perinatal brain injury following IUI. This supports a role for maternal CD8 + T-cell trafficking in placenta in mediating perinatal brain injury separate from preterm birth mechanisms.
Original language | English (US) |
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Article number | e12798 |
Journal | American Journal of Reproductive Immunology |
Volume | 79 |
Issue number | 5 |
DOIs | |
State | Published - May 2018 |
Keywords
- lipopolysaccharide
- lymphocyte trafficking
- neurobehavior
- placenta
- preterm birth
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Reproductive Medicine
- Obstetrics and Gynecology