Abstract

Simple SummaryThis study evaluated the effects of MIA elicited by porcine reproductive and respiratory syndrome virus and postnatal metabolic or immune stressors on chemical and inflammatory biomarkers in male and female pigs. Our results provide evidence that MIA interacting with postnatal stressors can have a long-lasting effect on the pig physiology, potentially affecting health, growth, and reproductive performance later in life.The effects of maternal immune activation (MIA) elicited by a prenatal stressor and postnatal metabolic or immune stressors on chemical and inflammatory biomarkers were studied in male and female pigs. Pigs exposed to MIA elicited by porcine reproductive and respiratory syndrome virus and matching controls were assigned at two months of age to fasting stress, immune stress, or a saline group. The serum levels of over 30 chemistry and immune analytes were studied. Significantly low levels of blood urea nitrogen were detected in females exposed to MIA, while the highest creatinine levels were identified in fasting females exposed to MIA. The levels of interferon gamma and interleukin 8 were highest in pigs exposed to postnatal immune challenge. The profiles suggest that MIA may sensitize pigs to postnatal stressors for some indicators while making them more tolerant of other stressors. Effectiveness of practices to ameliorate the impact of postnatal stressors on the physiology of the pig could be enhanced by considering the prenatal stress circumstances.

Highlights

  • The maternal immune response to infection or other stressors can result in fetal exposure to maternal inflammatory signals and stress hormones [1,2,3]

  • The objective of this study is to advance the understanding of the simultaneous effects of prenatal Porcine reproductive and respiratory syndrome virus (PRRSV)-elicited Maternal immune activation (MIA), postnatal fasting, and immune stressors and their interactions on biomarkers of physiological health and organ dysfunction in two-monthold pigs

  • The present study advances the understanding of the impact of prenatal MIA and postnatal stressors on blood biomarkers of physiological health and organ dysfunction

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Summary

Introduction

The maternal immune response to infection or other stressors can result in fetal exposure to maternal inflammatory signals and stress hormones [1,2,3]. Maternal immune activation (MIA) during gestation can alter fetal organ developmental and immune response processes leading to the disruption in peripheral immune and metabolic molecular levels [4,5]. 2 (IL-2) were detected in 7-day-old mice born from females that presented MIA elicited by the injection of the viral mimetic polyinosinic-polycytidylic acid (Poly(I:C)) during gestation [6]. With regard to metabolic indicators, serum non-esterified fatty acids concentrations were lower, and blood urine nitrogen concentrations were higher in heifers born from cows exposed to lipopolysaccharide immune challenge during gestation relative to control cows [7]. The double-hit hypothesis proposes that exposure to a first immune challenge during embryonic and fetal development (i.e., MIA)

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