Cumulative Physiological Events Influence the Inflammatory Response of the Bovine Udder to Escherichia coli Infections During the Transition Period

Abstract

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.

Effects of short-term feed restriction on milk yield and composition, and hormone and metabolite profiles in mid-lactation Sarda dairy sheep with different body condition score

“…During the Re-Fed period, NEFA concentration returned to initial levels. An increase in plasma concentration of NEFA is usually associated with impaired immune function both in cow (Burvenich et al, 2007) and sheep (Lacetera et al, 2001(Lacetera et al, , 2002, that could increase incidence of mastitis (Janosi et al, 2003) and milk SCC (Nyman et al, 2008). In our experiment, milk SCC was not statistically influenced by sampling (P=0.126).…”

Effects of continuous lactation and short dry periods on mammary function and animal health

“…Lower concentrations of natural protective factors are present in mammary secretions from glands producing large quantities of milk during late lactation (Smith et al, 1985b;Breau and Oliver, 1986); therefore, reduced milk production at dry-off for cows with SDP may provide higher concentration of these naturally protective factors. In addition, accumulation of a large volume of milk that increases the intramammary pressure and leakage of milk from the teats and facilitate bacterial penetration of the streak canal can be minimized by shortening DPL (Cousins et al, 1980;Burvenich et al, 2007). A positive correlation between the quantity of milk produced during late lactation and susceptibility to new IMI has been reported by others (Oliver et al, 1956).…”

Cell population, viability, and some key immunomodulatory molecules in different milk somatic cell samples in dairy cows

“…In the milk, striking changes occur in the morphology of PMN owing to the ingestion of fat globules and casein (Paape et al 1975;Paape & Guidry, 1977) by endocytosis. From this internalization of cell membrane result intracellular membrane bound vacuoles, a loss of pseudopodia, and cell rounding (Paape et al 2003;Rainard & Riollet, 2006;Burvenich et al 2007). These morphological and physiological changes consume a lot of energy which induces a decrease in phagocytic and bactericidal activity and, therefore, an impairment of the mammary gland defence (Paape et al 2003;Rainard & Riollet, 2006;Burvenich et al 2007).…”

“…From this internalization of cell membrane result intracellular membrane bound vacuoles, a loss of pseudopodia, and cell rounding (Paape et al 2003;Rainard & Riollet, 2006;Burvenich et al 2007). These morphological and physiological changes consume a lot of energy which induces a decrease in phagocytic and bactericidal activity and, therefore, an impairment of the mammary gland defence (Paape et al 2003;Rainard & Riollet, 2006;Burvenich et al 2007). Blood PMN have a short half-life (Carlson & Kaneko, 1975) and they spontaneously undergo apoptosis (Fadeel et al 1998;Smits et al 1999).…”