Inflammation and Calcium Homeostasis: Potential Implications for the TransitionPeriod

摘要

The vast majority of what we understand about calcium (Ca) homeostasis during the transition period was originally discovered by Dr. Ronald L. Horst (1949-2019) and his students/collaborators at the USDA National Animal Disease Center in Ames, IA. Atlactation onset, dairy cows experience a marked increase (>65%; DeGaris and Lean, 2008) in Ca requirements to support colostrum and milk synthesis (Horst et al., 2005). The dairy industry has long hypothesized that the mammary gland's Ca demand is so extensive and acute that it often exceeds the homeostatic mechanisms (i.e., parathyroid hormone [PTH] and Vitamin D) employed to replenish it and as a result clinical or subclinical hypocalcemia (SCH) occurs (Horst et al., 2005; Goff, 2008). Implementing therapeutic and prophylactic strategies (i.e., pre-calving acidifying rations) has markedly reduced the incidence of clinical hypocalcemia (Charbonneau et al., 2006; Reinhardt et al., 2011), but SCH remains common. Some consider post-calving SCH as "pathological" and assume it causal in a myriad of seemingly unrelated negative health outcomes (ketosis, poor reproduction, displaced abomasum [DA], immune suppression, etc.; Caixeta etal., 2017; Rodriguez etal., 2017; Neves etal., 2018a,b). We suggest (outlined below) that periparturient immune activation contributes to clinical and SCH and the low circulating Ca is a consequence (a reflection) of inflammation rather than a predictor of future problems. In fact, we hypothesize that many post-calving undesirable phenotypes (reduced dry matter intake [DMI], hypocalcemia, elevated non-esterified fatty acids [NEFA], hyperketonemia) are a consequence of immune activation and not themselves causative of transition cow maladies.