Conceptus mortality is greatest in mammals during the peri-implantation period, a time when conceptuses appose and attach to the uterine surface epithelium while releasing proinflammatory molecules. Interleukin 1 beta (IL1B), a master proinflammatory cytokine, is released by the primate, rodent, and pig blastocyst during the peri-implantation period and is believed to be essential for establishment of pregnancy. The gene encoding IL1B has duplicated in the pig, resulting in a novel gene. Preliminary observations indicate that the novel IL1B is specifically expressed by pig conceptuses during the peri-implantation period. To verify this, IL1B was cloned from mRNA isolated from Day 12 pig conceptuses and compared with IL1B cloned from mRNA isolated from pig peripheral blood leukocytes (PBLs). The pig conceptuses, but not the PBLs, expressed a novel IL1B, referred to here as interleukin 1 beta 2 (IL1B2). Porcine endometrium was treated with recombinant porcine interleukin 1 beta 1 (IL1B1), the prototypical cytokine, and IL1B2 proteins. Immunohistochemistry and real-time RT-PCR were used to measure activation of nuclear factor-kappa B (NFKB) and NFKB-regulated transcripts, respectively, within the endometrium. Both IL1B1 and IL1B2 activated NFKB in the uterine luminal epithelium within 4 h. The NFKB activation and related gene expression, however, were lower in endometrium treated with IL1B2, suggesting that the conceptus-derived cytokine may have reduced activity within the uterus. In conclusion, the peri-implantation pig conceptus expresses a novel IL1B that can activate NFKB within the uterine surface epithelium, likely creating a proinflammatory microenvironment during establishment of pregnancy in the pig.

No abstract

The objective was to determine if lactation affects fetal and placental development from day 28 to 42 of gestation. Bos taurus Holstein cows were assigned to one of the two treatments immediately after parturition (lactating (nZ23) or nonlactating (dried off immediately after calving; nZ20)). Cows were inseminated at w60 days postpartum with semen from a single ejaculate. Pregnant cows were slaughtered at 1 of 3 days of gestation (day 28, 35, or 42) and tissues were collected. The interval to first insemination, services per conception, and days to pregnancy were similar for lactating and nonlactating cows. Lactating cows had greater plasma GH and nonesterified fatty acids. Nonlactating cows had greater plasma glucose, insulin, and IGF1. There was no effect of lactation on plasma progesterone or estradiol concentrations. Lactation had a negative effect on the weight of the fetus and placenta (weights were less in lactating cows). Fetuses collected from cows that became pregnant after first insemination were heavier than fetuses collected from cows that became pregnant after second or third insemination. Pregnancy after first insemination was associated with greater blood glucose and IGF1 during the first 30 days postpartum. The conclusions were that lactation negatively affects the growth of fetal and placental tissues perhaps through a mechanism that involves hormones and metabolites that are affected by lactation. Fetal growth within cows conceiving at first insemination compared to second or third insemination was more rapid and was associated with greater blood glucose and IGF1 early postpartum (before day 30).

Glucose is an essential nutrient for the conceptus. The objective was to determine if lactation affected the amount of glucose crossing the placenta by measuring glucose and fructose in placental fluids in lactating and nonlactating cows. Holstein cows were assigned to one of 2 treatments immediately after parturition [lactating (n=23) or nonlactating (dried off immediately after calving; n=20)]. Pregnant cows were slaughtered at one of 3 d of pregnancy (d 28, 35, or 42) and tissues were collected. Plasma glucose and insulin were less in lactating cows. Pregnancies collected from lactating cows had less glucose and fructose in placental fluids compared with those from nonlactating cows. Relative to endometrium, the placenta expressed greater amounts of the glucose transporters SLC2A1 (Glut1), SLC2A3 (Glut3) and SLC2A4 (Glut4) mRNA. The mRNA for SLC2A1 decreased whereas the mRNA for SLC2A4 increased from d 28 to d 42 of pregnancy. Stepwise regression analyses for fetal and placental weight (dependent variable) retained day of pregnancy and maternal plasma insulin concentrations in the final model. The conclusion is that lower blood glucose and insulin in lactating cows may lead to less glucose crossing the placenta and slower fetal development during lactation. The slower fetal development may predispose lactating cows to fetal loss if developmental milestones are not reached.

No abstract