Characterizing the postnatal hypothalamic-pituitary-adrenal axis response of in utero heat stressed pigs at 10 and 15 weeks of age.

In utero heat stress alters postnatal physiological and behavioral stress responses in pigs. However, the mechanisms underlying these alterations have not been determined. The study objective was to characterize the postnatal hypothalamic-pituitary-adrenal axis response of in utero heat-stressed pigs. Pigs were subjected to a dexamethasone suppression test followed by a corticotrophin releasing hormone challenge at 10 and 15 weeks of age. Following the challenge, hypothalamic, pituitary, and adrenal tissues were collected from all pigs for mRNA abundance analyses. At 10 weeks of age, in utero heat-stressed pigs had a reduced (P < 0.05) cortisol response to the corticotrophin releasing hormone challenge versus controls. Additionally, the cortisol response tended to be greater overall (P < 0.10) in 15 versus 10-week-old pigs in response to the dexamethasone suppression test. The cortisol response tended to be reduced overall (P < 0.10) in 15 versus 10-week-old pigs in response to the corticotrophin releasing hormone challenge. Hypothalamic corticotropin releasing hormone mRNA abundance tended to be greater (P < 0.10) in in utero heat-stressed versus control pigs at 15-weeks of age. In summary, in utero heat stress altered some aspects of the hypothalamic-pituitary-adrenal axis related to corticotropin releasing hormone signaling, and age influenced this response.

In utero heat stress alters the postnatal innate immune response of pigs.

The effects of in utero heat stress (IUHS) range from decreased growth performance to altered behavior, but the long-term impact of IUHS on postnatal innate immune function in pigs is unknown. Therefore, the study objective was to determine the effects of early gestation IUHS on the immune, metabolic, and stress response of pigs subjected to an 8 hr lipopolysaccharide (LPS) challenge during postnatal life. Twenty-four pregnant gilts were exposed to thermoneutral (TN; n = 12; 17.5 ± 2.1 °C) or heat stress (HS; n = 12; cyclic 26 to 36 °C) conditions from days 6 to 59 of gestation, and then TN conditions (20.9 ± 2.3 °C) from day 60 of gestation to farrowing. At 12 wk of age, 16 IUHS and 16 in utero thermoneutral (IUTN) pigs were selected, balanced by sex and given an intravenous injection of LPS (2 µg/kg BW mixed with sterile saline [SAL] and injected at 2 µL/kg BW) or SAL (2 µL/kg BW). Body temperature was monitored every 30 min, and blood was obtained at 0, 1, 2, 3, 4, 6, and 8 hr following the LPS challenge. Blood samples were analyzed for glucose, insulin, non-esterified fatty acids (NEFA), cortisol, and cytokine concentrations. In addition, white blood cell counts were determined at 0 and 4 hr. Hour 0 data were used as covariates. Body temperature was increased (P < 0.01) in LPS (40.88 ± 0.08 °C) vs. SAL (39.83 ± 0.08 °C) pigs. Eosinophils tended to be decreased overall (P = 0.09; 43.9%) in IUHS vs. IUTN pigs. Glucose concentrations were reduced overall (P = 0.05; 5.9%) in IUHS vs. IUTN pigs. The NEFA concentrations tended to be greater (P = 0.07; 143.4%) in IUHS-LPS pigs compared with all other treatments, and IUTN-LPS pigs tended to have greater (127.4%) circulating NEFA concentrations compared with IUTN-SAL and IUHS-SAL pigs. Cortisol was increased (P = 0.04) in IUHS-LPS compared with IUTN-LPS pigs at 3 hr (21.5%) and 4 hr (64.3%). At 1 hr, tumor necrosis factor α was increased (P = 0.01; 115.1%) in IUHS-LPS compared with IUTN-LPS pigs. Overall, interleukin-1ß (IL-1ß) and interleukin-6 (IL-6) were greater (P < 0.04; 281.3% and 297.8%, respectively) in IUHS-LPS pigs compared with all other treatments, and IUTN-LPS pigs had increased IL-1ß and IL-6 concentrations compared with IUTN-SAL and IUHS-SAL pigs. In summary, IUHS altered the postnatal cytokine, metabolic, and physiological stress response of pigs during postnatal life, which may have negative implications toward the innate immune response of IUHS pigs to pathogens.

Fine mapping genetic variants associated with age at puberty and sow fertility using SowPro90 genotyping array.

Sow fertility traits, such as litter size and the number of lifetime parities produced (reproductive longevity), are economically important. Selection for these traits is difficult because they are lowly heritable and expressed late in life. Age at puberty (AP) is an early indicator of reproductive longevity. Here, we utilized a custom Affymetrix single-nucleotide polymorphisms (SNPs) array (SowPro90) enriched with positional candidate genetic variants for AP and a haplotype-based genome-wide association study to fine map the genetic sources associated with AP and other fertility traits in research (University of Nebraska-Lincoln [UNL]) and commercial sow populations. Five major quantitative trait loci (QTL) located on four Sus scrofa chromosomes (SSC2, SSC7, SSC14, and SSC18) were discovered for AP in the UNL population. Negative correlations (r = -0.96 to -0.10; P < 0.0001) were observed at each QTL between genomic estimated breeding values for AP and reproductive longevity measured as lifetime number of parities (LTNP). Some of the SNPs discovered in the major QTL regions for AP were located in candidate genes with fertility-associated gene ontologies (e.g., P2RX3, NR2F2, OAS1, and PTPN11). These SNPs showed significant (P < 0.05) or suggestive (P < 0.15) associations with AP, reproductive longevity, and litter size traits in the UNL population and litter size traits in the commercial sows. For example, in the UNL population, when the number of favorable alleles of an SNP located in the 3' untranslated region of PTPN11 (SSC14) increased, AP decreased (P < 0.0001), while LTNP increased (P < 0.10). Additionally, a suggestive difference in the observed NR2F2 isoforms usage was hypothesized to be the source of the QTL for puberty onset mapped on SSC7. It will be beneficial to further characterize these candidate SNPs and genes to understand their impact on protein sequence and function, gene expression, splicing process, and how these changes affect the phenotypic variation of fertility traits.

Evaluation and mitigation of the effects of in utero heat stress on piglet growth performance, postabsorptive metabolism, and stress response following weaning and transport.

In utero heat stress (IUHS) increases the energy requirements of pigs during postnatal life, and this may compound weaning and transport stress. The study objective was to evaluate and mitigate the negative effects of IUHS following weaning and transport through the provision of a nutrient-dense (ND) nursery diet formulated to meet the greater energy requirements of IUHS pigs during the first 14 d postweaning and transport. Twenty-four pregnant gilts were exposed to thermoneutral (TN; n = 12; 17.5 ± 2.1 °C) or heat stress (HS; n = 12; cycling 26 to 36 °C) conditions for the first half of gestation (day 6 to 59) and then TN conditions (20.9 ± 2.3 °C) until farrowing. Nine TN gilts and 12 HS gilts produced litters. At weaning (16.2 ± 0.4 d), mixed-sex piglets (N = 160; 4.78 ± 0.15 kg body weight [BW]) were transported (loading + transport + unloading) for 11 h 40 min. Following transport, piglets were blocked into pens (n = 4 pigs/pen) by in utero and dietary treatments: in utero thermoneutral (IUTN) + control (C) diet (n = 10 pens), IUTN + ND (n = 10 pens), IUHS + C (n = 10 pens), and IUHS + ND (n = 10 pens). Treatment diets were fed from day 1 to 14 postweaning and transport (period 1), and the C diet was fed to all pigs from day 14 to 35 postweaning and transport (period 2). Production measures were taken in 7 d intervals to calculate average daily gain (ADG), average daily feed intake (ADFI), average daily net energy intake (ADEI), gain:feed, and gain:net energy intake. Blood samples were collected prior to transport, following transport, and on days 2, 7, 14, 28, and 35 postweaning and transport to analyze cortisol, glucose, insulin, and nonesterified fatty acids. Behavior was assessed through video-recording on days 3, 5, 8, 11, and 13 postweaning and transport. In period 1, ADG was reduced (P = 0.04; 20.0 g/d) in IUHS vs. IUTN pigs. Pigs fed ND diets had reduced ADFI (P = 0.02; 9.3%) compared with C diet-fed pigs during period 1, which resulted in similar ADEI (P = 0.23; 1,115 ± 35 kcal/d). During transport, cortisol was decreased (P = 0.03; 25.8%) in IUHS vs. IUTN pigs. On day 2, glucose was decreased (P = 0.01; 13.8%) in IUHS vs. IUTN pigs. No in utero treatment-related behavior differences were observed but lying was reduced (P = 0.03; 6.5%) and standing was increased (P = 0.04; 14.1%) in ND vs. C pigs overall. In summary, IUHS reduced growth performance in pigs following weaning and transport, and providing an ND diet did not rescue the lost performance.

In utero heat stress alters postnatal phenotypes in swine.

The prenatal environment influences offspring health and development, and this is readily apparent when considering the well-described effects of maternal nutrition and stress on the postnatal metabolism, neural function, and stress response of progeny. Moreover, in laboratory species, sheep, and humans, the effects of in utero heat stress on offspring development have been described in detail for >50 years. Despite our extensive knowledge of the postnatal phenotypes elicited by in utero stressors, the carryover effects of in utero heat stress in pigs have only recently begun to be elucidated. The effects of climate change on increasing global temperatures, combined with greater metabolic heat production in modern swine, has increased heat stress susceptibility in pigs. Greater heat stress susceptibility can negatively affect swine welfare and performance and may impact future generations of pigs through in utero heat stress. Pigs exposed to in utero heat stress develop a variety of postnatal phenotypes that prevent profitable production, and compromise health, and welfare in commercial production systems. Specifically, in utero heat stress alters the postnatal stress response, core body temperature, response to an immune challenge, and is teratogenic. In addition, in utero heat stress changes postnatal body composition through reduced lean and increased adipose tissue accretion rates, respectively. Furthermore, in utero heat stress reduces piglet birth weight, body weight gain, and reproductive efficiency. Although the economic impact of in utero heat stress in pigs has yet to be determined, it likely rivals the postnatal consequences of heat stress and is a threat to the global sustainability of swine production.

Effects of mammalian in utero heat stress on adolescent body temperature.

In utero hyperthermia can cause a variety of developmental issues, but how it alters mammalian body temperature during adolescence is not well-understood. Study objectives were to determine the extent to which in utero hyperthermia affects future phenotypic responses to a heat load. Pregnant first parity pigs were exposed to thermal neutral (TN) or heat stress (HS) conditions during the entire gestation. Of the resultant offspring, 12 were housed in TN conditions, and 12 were maintained in HS conditions for 15 days. Adolescent pigs in HS conditions had increased rectal temperature and respiration rate (RR) compared to TN pigs, regardless of gestational treatment. Within the HS environment, no gestational difference in RR was detected; however, GHS pigs had increased rectal temperature compared to GTN pigs. As rectal temperature increased, GTN pigs had a more rapid increase in RR compared to the GHS pigs. Adolescent HS decreased nutrient intake, and body weight gain, but neither variable was statistically influenced by gestational treatments. In summary, in utero HS compromises the future thermoregulatory response to a thermal insult.