title: Innate immune response to intramammary infection with Serratia marcescens and Streptococcus uberis.
abstract: Streptococcus uberis and Serratia marcescens are 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 important, yet less well-studied, 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 beta, IL-8, IL-10, IL-12, IFN-gamma, TNF-alpha, sCD14, LBP, and the 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 beta, IL-10, IL-12, IFN-gamma, and C5a, relative to S. marcescens infection. Together, these data demonstrate the variability of the innate immune response to two distinct mastitis pathogens.
authors.affiliation: Bovine Functional Genomics Laboratory, Beltsville Agricultural Research Center, USDA-Agricultural Research Service, Beltsville, MD 20705, USA. dbanner@anri.barc.usda.gov
authors.forename: Douglas D
authors.initials: DD
authors.lastname: Bannerman
authors.forename: Max J
authors.initials: MJ
authors.lastname: Paape
authors.forename: Jesse P
authors.initials: JP
authors.lastname: Goff
authors.forename: Kayoko
authors.initials: K
authors.lastname: Kimura
authors.forename: John D
authors.initials: JD
authors.lastname: Lippolis
authors.forename: Jayne C
authors.initials: JC
authors.lastname: Hope
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism; D000818:Animals; D002199:Capillary Permeability; D002352:Carrier Proteins / Q000378:metabolism; D002417:Cattle; D002452:Cell Count / Q000662:veterinary; D015936:Complement C5a / Q000378:metabolism; D016207:Cytokines / Q000096:biosynthesis; D005260:Female; D005786:Gene Expression Regulation; D007774:Lactation; D007962:Leukocytes; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D008321:Mammary Glands, Animal / Q000098:blood supply / Q000382:microbiology; D008414:Mastitis, Bovine / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology; D008562:Membrane Glycoproteins / Q000378:metabolism; D008892:Milk / Q000166:cytology / Q000276:immunology / Q000382:microbiology; D016868:Serratia Infections / Q000276:immunology / Q000662:veterinary*; D012706:Serratia marcescens / Q000276:immunology*; D013290:Streptococcal Infections / Q000276:immunology / Q000662:veterinary*; D013997:Time Factors; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D002352:Carrier Proteins; D015936:Complement C5a; D016207:Cytokines; D018950:Lipopolysaccharide Receptors; D008562:Membrane Glycoproteins; D000099231:Lipopolysaccharide-Binding Protein