Department of Animal Sciences, Ohio Agricultural Research and Development Center, The Ohio State University, Wooster 44691.
Department of Animal Sciences, The Ohio State University, Columbus 43210.
J Dairy Sci. 2023 Apr;106(4):2642-2650. doi: 10.3168/jds.2022-22716. Epub 2023 Feb 22.
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.
非泌乳期乳腺的乳腺内感染很常见，可发生在乳腺上皮细胞（MEC）快速积累的时期，这可能最终会减少总 MEC 数量。MEC 数量减少，源于 MEC 增殖受损和细胞凋亡增加，预计会降低未来的产奶量。本研究的目的是测量在快速生长的激素诱导未感染和金黄色葡萄球菌感染的乳腺中，上皮和基质区室的细胞增殖和凋亡程度。11 至 14 月龄的非妊娠小母牛（n = 8）接受超生理剂量的雌二醇和孕酮注射 14 天。每头小母牛的一个乳腺随机接受金黄色葡萄球菌（CHALL）灌注，而另一个乳腺则在注射第 8 天被指定为未感染对照。在激素注射的最后一天，从小牛的中心和边缘实质区采集乳腺组织，并通过 Ki-67 染色评估增殖，通过末端脱氧核苷酸转移酶 dUTP 缺口末端标记法评估凋亡。CHALL 和未感染对照象限之间的细胞增殖差异不明显，但边缘实质中的 MEC 增殖略高于中心实质。巧合的是，CHALL 象限经历了更多的凋亡 MEC 和更少的基质细胞凋亡，而未感染对照象限则经历了更多的凋亡 MEC 和更少的基质细胞凋亡。本研究还首次深入了解了允许乳腺脂肪垫被扩张的乳腺上皮替代的机制，因为边缘实质中的凋亡基质细胞百分比高于中心实质。综合来看，这些数据表明金黄色葡萄球菌乳腺内感染通过减少 MEC 数量并阻止其向乳腺脂肪垫扩张来损害乳腺上皮生长。在快速乳腺生长期间，这些因素预计会损害初乳产奶量。
