Investigating milk cell population changes in response to heat stress and characterizing functionality of epithelial cells in milk of lactating dairy cows

Abstract

Understanding the number of mammary epithelial cells a cow maintains is essential to maximize milk synthesis in lactating dairy cows. This thesis aimed to investigate milk cell population changes in lactating dairy cows in response to heat stress (HS) using a pair-feeding model (PFTN). Additionally, this thesis explored the potential role of mammary epithelial cells in milk of lactating dairy cows as phagocytic cells capable of efferocytosing apoptotic mammary epithelial cells. The first study evaluated cell shedding into milk in response to nine days of HS or PFTN. There was a decline in dry matter intake (DMI) and milk yield (MY) in response to HS and pair-feeding. Milk yield decreased over 9 days for both treatments and PFTN cows had a greater MY on d 2,7, and 8 compared to HS cows. The concentration of MEC shed into milk did not change after nine days of HS or PFTN and there were no differences between groups. There was a lower concentration of immune cells in milk from HS cows and a higher concentration of BTN+CD45-CD14+ cells than PFTN cows. The second study examined the potential role of mammary epithelial cells as phagocytes in consuming apoptotic mammary epithelial cells during lactation. Mammary epithelial cells act as non-professional phagocytes during the dry period to aid in maintaining tissue homeostasis. The role of mammary epithelial cells as phagocytes during lactation in dairy cows hasn't received investigation. In this study, mammary epithelial cells in milk consumed cultured apoptotic mammary epithelial cells under in vitro conditions. Factors that influence mammary epithelial cell shedding into milk play an important role in milk production. By investigating factors that affect cell shedding into milk we can better understand the dynamics of the mammary gland and potentially improve milk production and lactation persistency in cows.