Burvenich C, Bannerman D D, Lippolis J D, Peelman L, Nonnecke B J, Kehrli M E, Paape M J
Ghent University, Faculty of Veterinary Medicine, Laboratory of Physiology, B9820 Merelbeke, Belgium.
J Dairy Sci. 2007 Jun;90 Suppl 1:E39-54. doi: 10.3168/jds.2006-696.
A high proportion of intramammary coliform infections present at parturition develop disease characterized by severe inflammatory signs and sepsis during the first 60 to 70 d of lactation. In the lactating bovine mammary gland, the innate immune system plays a critical role in determining the outcome of these infections. Since the beginning of the 1990s, research has increased significantly on bovine mammary innate defense mechanisms in connection with the pathogenesis of coliform mastitis. Neutrophils are key effector cells of the innate immune response to intramammary infection, and their function is influenced by many physiological events that occur during the transition period. Opportunistic infections occur when the integrity of the host immune system is compromised by physical and physiological conditions that make the host more susceptible. The innate immune system of many periparturient cows is immunocompromised. It is unlikely that periparturient immunosuppression is the result of a single physiological factor; more likely, several entities act in concert, with profound effects on the function of many organ systems of the periparturient dairy cow. Their defense system is unable to modulate the complex network of innate immune responses, leading to incomplete resolution of the pathogen and the inflammatory reaction. During the last 30 yr, most efforts have been focused on neutrophil diapedesis, phagocytosis, and bacterial killing. How these functions modulate the clinical outcome of coliform mastitis, and how they can be influenced by hormones and metabolism has been the subject of intensive research and is the focus of this review. The afferent (sensing) arm of innate immunity, which enables host recognition of a diverse array of pathogens, is the subject of intense research interest and may contribute to the variable inflammatory response to intramammary infections during different stages of lactation. The development of novel interventions that modulate the inflammatory response or contribute to the elimination of the pathogen or both may offer therapeutic promise in the treatment of mastitis in periparturient cows.
分娩时出现的大量乳房内大肠埃希菌感染,在泌乳的最初60至70天会发展为以严重炎症体征和败血症为特征的疾病。在泌乳期奶牛的乳腺中,先天免疫系统在决定这些感染的结果方面起着关键作用。自20世纪90年代初以来,关于与大肠埃希菌性乳腺炎发病机制相关的奶牛乳腺先天防御机制的研究显著增加。中性粒细胞是乳房内感染先天免疫反应的关键效应细胞,其功能受围产期发生的许多生理事件影响。当宿主免疫系统的完整性因使宿主更易感染的物理和生理状况而受损时,就会发生机会性感染。许多围产期奶牛的先天免疫系统受到免疫抑制。围产期免疫抑制不太可能是单一生理因素的结果;更有可能的是,几个因素共同起作用,对围产期奶牛许多器官系统的功能产生深远影响。它们的防御系统无法调节先天免疫反应的复杂网络,导致病原体和炎症反应无法完全消除。在过去30年中,大多数研究都集中在中性粒细胞的渗出、吞噬作用和细菌杀伤上。这些功能如何调节大肠埃希菌性乳腺炎的临床结果,以及它们如何受到激素和代谢的影响,一直是深入研究的主题,也是本综述的重点。先天免疫的传入(传感)臂能够使宿主识别多种病原体,是研究的热点,可能导致泌乳不同阶段对乳房内感染的炎症反应存在差异。开发能够调节炎症反应或有助于消除病原体或两者兼有的新型干预措施,可能为治疗围产期奶牛乳腺炎提供治疗前景。