Summary Objectives were to investigate mechanisms by which a nutritional supplement alters immunity in dairy cattle. Our hypothesis was that feeding this product to dairy cattle altered neutrophil gene expression. Eight periparturient Jersey cattle were randomly assigned to one of two treatments: control and treated. Control animals were fed a dry cow ration for 1 month prior to calving. The treated cows were fed the same ration supplemented with OmniGen‐AF. Following calving, blood samples were taken and neutrophils were prepared after which RNA was extracted. Gene expression in neutrophils of treated versus control‐fed animals was then assessed using bovine‐total leukocyte (BOTL‐5) arrays. Eighteen genes were differentially regulated in the experimental group and of these, twice as many were up‐regulated as down‐regulated. Patterns of changes indicated that the additive might alter neutrophil apoptosis, signaling and sensitivity. Two of the regulated genes [interleukin‐1β converting enzyme (ICE) and interleukin‐4 receptor (IL‐4R)] were investigated in more detail using quantitative reverse transcriptase‐polymerase chain reaction (QRT‐PCR). Each was found to be elevated by the feeding of experimental product. Increased expression of ICE indicates potential for enhanced neutrophil expression of interleukin‐1β (IL‐1β), a cytokine which plays roles in the inflammatory response and which stimulates adaptive immunity following innate immune activation. Altered expression of IL‐4R indicates potential for changes in neutrophil apoptosis. The experiment identified mechanisms by which the additive altered neutrophil gene expression. While many nutrients support the immune system, we have shown that a non‐traditional nutritional approach may also have utility in modulating immune function.

The goal of this study was to examine the ability of a commercially available feed additive (OmniGen-AF) to reduce mammary infections caused by a single strain of mastitic pathogens (Streptococcus uberis, Escherichia coli, Staphylococcus aureus and Klebsiella pneumoniae) and to examine the effects of the additive on markers of mammary immunity. Four experiments were completed using a murine model of bovine mastitis. Infection progression was examined using Sybr-green-and TaqMan-based quantitative PCR assays of 16S ribosomal DNA. Infection of the mammary gland with all pathogens caused rapid (24 to 48 h) appearance of pathogen DNA in mammary tissue. Provision of the feed additive for 2 weeks before infection significantly (P , 0.05) reduced the extent of pathogen DNA accumulation in models of S. uberis, E. coli and S. aureus infection. The additive was ineffective in reducing mammary infections caused by K. pneumoniae. We examined mechanisms of action of the additive through assessment of mammary concentrations of mammary myeloperoxidase (MPO), major histocompatibility complex 2 class II (MHC) and macrophage inflammatory protein-1a (MIP) messenger RNA (mRNA) concentrations and by examining serum complement C3 concentration. Infection of the mammary gland increased concentrations of MPO and MHC mRNAs (P , 0.05). Ability of the pathogen to elicit changes in mammary MPO and MHC gene expression was enhanced by the provision of the additive for 2 weeks before infection. These data imply that the additive increased the mammary inflammatory response and increased antigen presentation during a mammary infection. Value of the additive in preventing mastitis in cattle awaits additional studies using a bovine model and further evaluation of additional strains of the pathogens used in this study.

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