Abstract #312

# 312
Maternal late-gestation metabolic stress is associated with changes in immune and metabolic responses of dairy calves.
Tahlia Ling2, Marta Hernandez-Jover2,3, Lorraine M. Sordillo1, Angel Abuelo*1,3, 1Michigan State University, Department of Large Animal Clinical Sciences, East Lansing, MI, 2Charles Sturt University, School of Animal and Veterinary Sciences, Wagga Wagga, NSW, Australia, 3Graham Centre for Agricultural Innovation (Charles Sturt University and NSW Department of Primary Industries), Wagga Wagga, NSW, Australia.

This study aimed to investigate if metabolic stress in late gestation dairy cows is associated with changes in the metabolic and immune responses of their offspring during the first month of life. Holstein-Friesian cows (n = 12) were blood sampled at 28 and 15 d before expected calving. The average between these 2 sampling points in the concentrations of nonesterified fatty acids (NEFA), haptoglobin (Hp), and oxidative stress index (OSi) were calculated as indicators of lipid mobilization, inflammation, and oxidative stress (OS), respectively. Calves received 4 L of colostrum from their respective dams within 12 h of life and were classified into groups (n = 6 each) according to their dams’ high or low degree of lipid mobilization, inflammation, and OS. The metabolic responses of calves in each of these groups were compared weekly up to 1 mo by assessing serum concentration of NEFA, Hp, and OSi. Additionally, whole blood at each sampling was subjected to a LPS-stimulated TNFα production assay to assess cell-mediated innate immunity against induced inflammatory responses. Mixed models with repeated measures were used. Calves born to cows with higher NEFA or OSi showed significantly lower birthweights, whereas no association between maternal metabolic stress groups and ADG was identified. Calves exposed to high maternal OS had higher concentrations of Hp (P = 0.013) and TNFα (P = 0.031), indicating greater basal inflammatory responses. In contrast, LPS-induced inflammatory responses were less robust in calves exposed to higher maternal Hp and OSi (Table 1), suggesting compromised immune responses. Collectively, these data suggest that prenatal exposure to maternal metabolic stress may adversely impact some metabolic and inflammatory responses of the offspring that could influence disease susceptibility. Table 1. TNFα release according to the degree of maternal OSi1
10 ng/mL LPS stimulation5 μg/mL LPS stimulation
Low OSiHigh OSiLow OSiHigh OSi
Wk 1136.1±12.5351.8±8.01*243.7±20.6595.4±13.27**
Wk 2117.2±11.4724.3±4.55**313.9±24.67155.3±13.49**
Wk 387.19±5.9939.7±6.89*362.2±22.00217.4±15.59**
Wk 472.9±2.9232.0±5.62*445.3±14.07274.9±21.19**
1Results expressed in percentage increase from control concentration (mean±SE).

Key Words: calf health, metabolic stress