| First Author | Uehre GM | Year | 2023 |
| Journal | Int J Mol Sci | Volume | 24 |
| Issue | 22 | PubMed ID | 38003279 |
| Mgi Jnum | J:343242 | Mgi Id | MGI:7563228 |
| Doi | 10.3390/ijms242216091 | Citation | Uehre GM, et al. (2023) B Cells Induce Early-Onset Maternal Inflammation to Protect against LPS-Induced Fetal Rejection. Int J Mol Sci 24(22) |
| abstractText | The maternal balance between B regulatory (Breg) cells and inflammatory B cells is of central importance for protection against preterm birth (PTB). However, the impact of B cell signaling in early maternal and fetal immune responses on inflammatory insults remains underinvestigated. To understand which role B cells and B-cell-specific signaling play in the pathogenesis of PTB, the later was induced by an injection of LPS in B cell-sufficient WT mice, CD19(-/-), BMyD88(-/-) and microMT murine dams at gestational day 16 (gd 16). WT dams developed a strong inflammatory response in their peritoneal cavity (PC), with an increased infiltration of granulocytes and enhanced IL-6, TNF-alpha, IL-17 and MCP-1 levels. However, they demonstrated a reduced NOS2 expression of PC macrophages 4 h after the LPS injection. Simultaneously, LPS-challenged WT dams upregulated pregnancy-protective factors like IL-10 and TARC. The concentrations of inflammatory mediators in the placental supernatants, amniotic fluids, fetal serums and gestational tissues were lower in LPS-challenged WT dams compared to CD19(-/-), BMyD88(-/-) and microMT dams, thereby protecting WT fetuses from being born preterm. B cell deficiency, or the loss of B-cell-specific CD19 or MyD88 expression, resulted in an early shift from immune regulation towards inflammation at the fetomaternal interface and fetuses, resulting in PTB. |
