Maternal B cell signaling orchestrates fetal development in mice.
Animals
Antigens, CD19
/ genetics
B-Lymphocytes
/ metabolism
Female
Fetal Development
Fetus
/ embryology
Interleukin-10
/ deficiency
Mice
Mice, Inbred BALB C
Mice, Knockout
Myeloid Differentiation Factor 88
/ deficiency
Pregnancy
Signal Transduction
Uterine Artery
/ metabolism
Uterus
/ blood supply
Vascular Resistance
B cells
B10 cells
High frequency ultrasound imaging
Intrauterine development
Mouse
MyD88
Preterm birth
Journal
Development (Cambridge, England)
ISSN: 1477-9129
Titre abrégé: Development
Pays: England
ID NLM: 8701744
Informations de publication
Date de publication:
15 04 2022
15 04 2022
Historique:
received:
06
05
2021
accepted:
25
08
2021
pubmed:
17
9
2021
medline:
3
2
2022
entrez:
16
9
2021
Statut:
ppublish
Résumé
B cell participation in early embryo/fetal development and the underlying molecular pathways have not been explored. To understand whether maternal B cell absence or impaired signaling interferes with placental and fetal growth, we paired CD19-deficient (CD19-/-) mice, females with B cell-specific MyD88 (BMyD88-/-) or IL10 (BIL10-/-) deficiency as well as wild-type and MyD88-/- controls on C57Bl/6 background with BALB/c males. Pregnancies were followed by ultrasound and Doppler measurements. Implantation number was reduced in BMyD88-/- and MyD88-/- mice. Loss of MyD88 or B cell-specific deletion of MyD88 or IL10 resulted in decreased implantation areas at gestational day (gd) 5, gd8 and gd10, accompanied by reduced placental thickness, diameter and areas at gd10. Uterine artery resistance was enhanced in BIL10-/- dams at gd10. Challenge with 0.4 mg lipopolysaccharide/kg bodyweight at gd16 revealed that BMyD88-/-, BIL10-/- and CD19-/- mothers delivered preterm, whereas controls maintained their pregnancy. B cell-specific MyD88 and IL10 expression is essential for appropriate in utero development. IL10+B cells are involved in uterine blood flow regulation during pregnancy. Finally, B cell-specific CD19, MyD88 and IL10 expression influences susceptibility towards preterm birth.
Identifiants
pubmed: 34528666
pii: 272200
doi: 10.1242/dev.199783
pii:
doi:
Substances chimiques
Antigens, CD19
0
CD19 antigen, mouse
0
IL10 protein, mouse
0
Myd88 protein, mouse
0
Myeloid Differentiation Factor 88
0
Interleukin-10
130068-27-8
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2021. Published by The Company of Biologists Ltd.
Déclaration de conflit d'intérêts
Competing interests The authors declare no competing or financial interests.