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.

This study determined whether supplementing the diets of dairy cows during the peripartum period with organic trivalent Cr influenced the capacity of their peripheral blood mononuclear cells to produce activation cytokines in response to stimulation with mitogens in vitro. Nine cows were fed 0.5 ppm of Cr/d per cow from 6 wk prepartum to 16 wk postpartum; 10 other periparturient cows served as unsupplemented controls. Mononuclear leukocytes, enriched from peripheral blood during wk 0, 2, 4, and 6 of lactation, were cultured with or without the T-lymphocyte mitogen, concanavalin A. Culture supernatants, harvested at 24, 48, or 72 h, were assayed for interleukin-2, interferon-gamma, and tumor necrosis factor-alpha. The cytokines were barely detectable in the supernatants from the unstimulated cultures, but supernatants from mitogen-stimulated cultures contained higher concentrations of each cytokine. For cows fed Cr, concentrations of all three cytokines in the culture supernatants of the mitogen-stimulated mononuclear cells decreased significantly relative to values for unsupplemented cows, particularly around peak lactation for the 24- and 48-h cultures. Theses results extended our previous observations and supported the hypothesis that organic Cr is immunomodulatory in high producing cows.