Utero-Placental Immune Milieu during Normal and Aglepristone-Induced Parturition in the Dog
Maternal immunotolerance is required for the maintenance of pregnancy, in sharp contrast with the uterine pro-inflammatory activity observed during parturition in several species. Correspondingly, in the dog, increased immune signaling at term has been suggested, but a deeper understanding of the ut...
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Veröffentlicht in: | Animals (Basel) 2021-12, Vol.11 (12), p.3598 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Maternal immunotolerance is required for the maintenance of pregnancy, in sharp contrast with the uterine pro-inflammatory activity observed during parturition in several species. Correspondingly, in the dog, increased immune signaling at term has been suggested, but a deeper understanding of the uterine immune milieu is still missing. Thus, the availability of 30 immune-related factors was assessed in utero-placental samples collected during post-implantation (days 18-25 of pregnancy) and mid-gestation (days 35-40) stages, and at the time of prepartum luteolysis. Gene expression and/or protein localization studies were employed. Samples collected from antigestagen (aglepristone)-treated dogs were further analyzed. Progression of pregnancy was associated with the downregulation of
and upregulation of
(
< 0.05) at mid-gestation. When compared with mid-gestation, a higher availability of several factors was observed at term (e.g.,
,
,
). However, in contrast with natural parturition,
,
,
,
,
and
were upregulated after aglepristone treatment (
< 0.05), but not
or
(
> 0.05). Altogether, these results show an increased immune activity during canine parturition, involving, i.a., M2 macrophages, Treg and Th cells, with strong support for progesterone-mediated immunomodulation. Furthermore, differences between term and induced parturition/abortion could relate to differences in placental maturation towards parturition and/or functional traits of antigestagens. |
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ISSN: | 2076-2615 2076-2615 |
DOI: | 10.3390/ani11123598 |