Costa A, Bovenhuis H, Egger-Danner C, Fuerst-Waltl B, Boutinaud M, Guinard-Flament J, Obritzhauser W, Visentin G, Penasa M
Department of Veterinary Medical Sciences, University of Bologna, 40064 Ozzano dell'Emilia (BO), Italy.
Animal Breeding and Genomics Group, Wageningen University, 6700 AH Wageningen, the Netherlands.
J Dairy Sci. 2025 Jan;108(1):635-650. doi: 10.3168/jds.2024-25467. Epub 2024 Sep 27.
Milk lactose content (LC) physiologically decreases with parity order in dairy cows, but also after udder health inflammation(s) and in presence of elevated milk SCC in subclinical cases. Therefore, the progressive decrease in milk LC observed along cows' productive life can be attributed to a combination of factors that altogether impair the epithelial integrity, resulting in weaker tight junctions, e.g., physiological aging of epithelium, mechanical epithelial stress due to milking, and experienced clinical or subclinical mastitis. Mastitis is also known to affect the udder synthesis ability, so our intention through this study was to evaluate if there is a cumulative and lasting effect of mammary gland inflammation(s) on milk yield (MY) and LC. For this purpose, we used diagnoses of clinical mastitis and milk data of Austrian Fleckvieh cows to evaluate the effect of cumulative mastitis events on LC and MY. Only mastitis diagnoses recorded by trained veterinarians were used. Finally, we investigated if cumulative mastitis is a heritable trait and whether it is genetically correlated with either LC or MY. Estimates were obtained using univariate and bivariate linear animal models. A significant reduction in LC and MY was observed in cows that suffered from mastitis compared with those that did not experience udder inflammation. The h of cumulative mastitis is promising and much greater (0.09) than the h of the binary event itself (≤0.03). The genetic correlations between cumulative mastitis with LC and MY were negative, suggesting that cows with a great genetic merit for MY and LC are expected to be more resistant to repeated inflammations and less recidivist. When we used number of lifetime SCC peaks (≥200,000 or 400,000 cells/mL) to calculate cumulative inflammation events, h was even higher (up to 0.38), implying that subclinical mastitis also has a relevant negative impact on both LC and MY. Finally, the present study demonstrated how repeated mastitis events can permanently affect the mammary gland epithelial integrity and synthesis ability, and that the number of cumulative mastitis is a promising phenotype to be used in selection index in combination with other indicator traits toward more resistant and resilient mammary glands.
奶牛的乳乳糖含量（LC）在生理上会随着胎次增加而降低，在乳房健康出现炎症后以及亚临床病例中乳体细胞数（SCC）升高时也会降低。因此，在奶牛的整个生产周期中观察到的乳LC逐渐下降，可能是多种因素共同作用的结果，这些因素共同损害了上皮完整性，导致紧密连接变弱，例如上皮的生理性老化、挤奶引起的机械性上皮应激，以及经历过临床或亚临床乳腺炎。乳腺炎还已知会影响乳房的合成能力，因此我们开展本研究的目的是评估乳腺炎症对产奶量（MY）和LC是否存在累积和持久的影响。为此，我们利用奥地利弗莱维赫奶牛的临床乳腺炎诊断和产奶数据，来评估累积乳腺炎事件对LC和MY的影响。仅使用经过培训的兽医记录的乳腺炎诊断结果。最后，我们研究了累积乳腺炎是否是一种可遗传的性状，以及它与LC或MY是否存在遗传相关性。估计值通过单变量和双变量线性动物模型获得。与未经历乳房炎症的奶牛相比，患有乳腺炎的奶牛的LC和MY显著降低。累积乳腺炎的遗传力前景良好，且比二元事件本身的遗传力（≤0.03）大得多（0.09）。累积乳腺炎与LC和MY之间的遗传相关性为负，这表明在MY和LC方面具有良好遗传优势的奶牛预计对反复炎症更具抵抗力，复发率更低。当我们使用一生SCC峰值数量（≥200,000或400,000个细胞/毫升）来计算累积炎症事件时，遗传力甚至更高（高达0.38），这意味着亚临床乳腺炎对LC和MY也有相关的负面影响。最后，本研究证明了反复的乳腺炎事件如何永久性地影响乳腺上皮完整性和合成能力，并且累积乳腺炎的数量是一个有前景的表型，可与其他指标性状结合用于选择指数，以培育更具抵抗力和恢复力的乳腺。
