Inhibition of mTOR in bovine monocyte derived macrophages and dendritic cells provides a potential mechanism for postpartum immune dysfunction in dairy cows.

Dairy cattle experience a profound nutrient deficit postpartum that is associated with immune dysfunction characterized by heightened inflammation and reduced pathogen clearance. The activation of the central nutrient-sensing mTOR pathway is comparatively reduced in leukocytes of early postpartum dairy cows during this time of most pronounced nutrient deficit. We assessed the effect of pharmacological mTOR inhibition (Torin-1, rapamycin) on differentiation of monocyte derived classically (M1) and alternatively (M2) activated macrophages (MPh) and dendritic cells (moDC) from 12 adult dairy cows.

The effect of ex vivo lipopolysaccharide stimulation and nutrient availability on transition cow innate immune cell AKT/mTOR pathway responsiveness.

Postpartum dairy cows experience a heightened inflammatory state coinciding with the time of greatest nutrient deficit. Nutrient availability is sensed on the cellular level by nutrient sensing kinases, such as the PI3K/AKT/mTOR (mTOR) pathway, a key orchestrator of immune cell activation and inflammatory balance. Our objective was to determine the responsiveness of this pathway to inflammatory stimulation with and without nutrient supplementation ex vivo.

The degree of postpartum metabolic challenge in dairy cows is associated with peripheral blood mononuclear cell transcriptome changes of the innate immune system.

Dairy cows undergo a nutrient deficit immediately postpartum when lactational demands exceed nutrient intake. This occurs concurrently to an increased challenge due to bacterial and viral infections, yet ability for pathogen clearance is reduced despite a heightened and often host-damaging inflammatory response. We hypothesized that nutrient stress is associated with differences in the immune cell transcriptome.

Location-specific expression of chemokines, TNF-α and S100 proteins in a teat explant model.

The distal compartments of the udder are the first to interact with invading pathogens. The regulatory and effector functions of two major teat regions [Fürstenberg's rosette (FR); teat cistern (TC)] are largely unknown. The objective of this study was to establish an in vitro model with explants of the FR and the TC to analyse their response towards Escherichia coli LPS and Staphylococcus aureus lipoteichoic acid (LTA).