|HOPE, JAYNE - INST FOR ANIMAL HEALTH
Submitted to: Veterinary Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/27/2004
Publication Date: 11/10/2004
Citation: Bannerman, D.D., Paape, M.J., Goff, J.P., Kimura, K., Lippolis, J.D., Hope, J.C. 2004. Innate immune response to intramammary infection with serratia marcessens and streptococcus uberis. Veterinary Research. 35(6):681-700.
Interpretive Summary: Streptococcus uberis and Serratia marcescens are common environmental mastitis pathogens. As control practices continue to diminish the incidence of mastitis induced by contagious pathogens, the proportion of mastitis cases caused by environmental pathogens continues to increase. Environmental pathogens are fairly ubiquitous and can be isolated from feces, bedding, soil, and water. Antibiotic treatment against many environmental pathogens remains sub-optimal. The ability of bacteria to establish successful infection is due, in part, to the nature of the immune response mounted against these invading pathogens. This study increases our understanding of mammary host defense mechanisms to the environmental pathogens Streptococcus uberis and Serratia marcescens, and identifies both common and divergent innate immune responses elicited by these bacteria.
Technical Abstract: Streptococcus uberis and Serratia marcescens are common Gram-positive and Gram-negative bacteria, respectively, that induce clinical mastitis. Once initial host barrier systems have been breached by these pathogens, the innate immune system provides the next level of defense against these infectious agents. The innate immune response is characterized by the induction of pro-inflammatory cytokines, as well as, increases in other accessory proteins that facilitate host recognition and elimination of the pathogens. The objective of the current study was to characterize the innate immune response during clinical mastitis elicited by these two distinct Gram-positive and Gram-negative organisms. The pro-inflammatory cytokine response and changes in the levels of the innate immune accessory recognition proteins, soluble CD14 (sCD14) and lipopolysaccharide (LPS)-binding protein (LBP), were studied. Decreased milk output, induction of a febrile response, and increased acute phase synthesis of LBP were all characteristic of the systemic response to intramammary infection with either organism. Infection with either bacteria similarly resulted in increased milk levels of IL-1', IL-8, IL-10, IL-12, IFN-', TNF-', sCD14, LBP, and the activated complement component, C5a. However, the duration of and/or maximal changes in the increased levels of these inflammatory markers were significantly different for several of the inflammatory parameters assayed. In particular, S. uberis infection was characterized by the sustained elevation of higher milk levels of IL-1', IL-10, IL-12, IFN-', and C5a, relative to S. marcescens infection. Together, these data demonstrate the variability of the innate immune response to two distinct and dissimilar mastitis pathogens.