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Updated: Aug 9, 2025
Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
Published on: January 17, 2025
Cellular proliferation and apoptosis in Staphylococcus aureus-infected heifer mammary glands experiencing rapid
Pari H Baker1, Kellie M Enger1, Sheila K Jacobi2
1Department of Animal Sciences, Ohio Agricultural Research and Development Center, The Ohio State University, Wooster 44691.
Abstract:
Intramammary infections in nonlactating mammary glands are common and can occur during periods of rapid mammary epithelial cell (MEC) accumulation, which may ultimately reduce total MEC numbers. Reduced MEC numbers, resulting from impaired MEC proliferation and increased cellular apoptosis, are expected to reduce future milk yields. The objective of this study was to measure the degree of cellular proliferation and apoptosis in the epithelial and stromal compartment of uninfected and Staphylococcus aureus-infected mammary glands hormonally induced to grow rapidly. Nonpregnant heifers (n = 8) between 11 and 14 mo of age were administered supraphysiological injections of estradiol and progesterone for 14 d. One mammary gland of each heifer was randomly selected and infused with Staph. aureus (CHALL) while another mammary gland was designated as an uninfected control on d 8 of injections. Mammary tissues were collected on the last day of hormonal injections from center and edge parenchymal regions and subject to proliferation assessment via Ki-67 staining and apoptotic assessment via terminal deoxynucleotidyl transferase dUTP nick-end labeling. Differences in cellular proliferation between CHALL and uninfected control quarters were not apparent, but proliferation of MEC was marginally greater in edge parenchyma than in center parenchyma. Coincidently, CHALL quarters experienced a greater percentage of apoptotic MEC and lower percentage of stromal cells undergoing apoptosis than uninfected control quarters. This study also provides the first insight into the mechanisms that allow the mammary fat pad to be replaced by expanding mammary epithelium as edge parenchyma contained a greater percentage of apoptotic stromal cells than center parenchyma. When taken together, these data suggest that Staph. aureus intramammary infection impairs mammary epithelial growth through reductions in MEC number and by preventing its expansion into the mammary fat pad. These factors during periods of rapid mammary growth are expected to impair first lactation milk yield.
Insights
Staphylococcus aureus infection in developing mammary glands increases mammary epithelial cell apoptosis, potentially reducing future milk production. This study investigated infection effects on cell growth during rapid mammary development in heifers.
Area of Science:
- Veterinary Medicine
- Animal Science
- Reproductive Biology
Background:
- Intramammary infections (IMIs) during nonlactating periods can decrease mammary epithelial cell (MEC) numbers.
- Reduced MEC numbers, due to impaired proliferation and increased apoptosis, are linked to lower future milk yields.
Purpose of the Study:
- To quantify cellular proliferation and apoptosis in epithelial and stromal compartments of hormonally stimulated mammary glands infected with Staphylococcus aureus (Staph. aureus).
- To understand the impact of Staph. aureus infection on MECs and stromal cells during rapid mammary growth in heifers.
Main Methods:
- Nonpregnant heifers received supraphysiological estradiol and progesterone injections for 14 days to induce mammary growth.
- One mammary gland was infused with Staph. aureus (CHALL), while another served as an uninfected control.
- Mammary tissues were analyzed for MEC proliferation (Ki-67) and apoptosis (TUNEL) in center and edge parenchyma.
Main Results:
- No significant difference in overall cellular proliferation between infected and control glands.
- Mammary epithelial cells (MECs) showed higher apoptosis in Staph. aureus-infected glands compared to controls.
- Stromal cell apoptosis was lower in infected glands, particularly in the center parenchyma.
Conclusions:
- Staph. aureus infection during rapid mammary growth impairs MEC number and expansion into the mammary fat pad.
- Increased MEC apoptosis and altered stromal cell apoptosis suggest infection negatively impacts mammary development.
- These effects are predicted to reduce first lactation milk yield in affected heifers.
