Enhancing dietary cation-anion difference reshaped the distribution of endotoxin across different biofluids and influenced inflammatory response in dairy cows exposed to heat stress

Abstract

The objective of the present study was to investigate the alterations of lipopolysaccharide (LPS) endotoxin across four different biofluids (i.e., rumen fluid, blood plasma, milk, and urine) and LPS-related inflammation responses in Holstein dairy cows under heat stress through the regulation of dietary cation-anion difference (DCAD). Eight lactating Holstein dairy cows were randomly assigned in a 2 × 2 crossover design to either a control DCAD diet (CON: 33.5 mEq/100 g DM) or a high DCAD diet (HDCAD: 50.8 mEq/100 g DM), and each experimental period lasted for 21 days. Samples of rumen fluid, blood plasma, milk, and urine were collected on the last day of each period and the concentrations of LPS endotoxin in those samples were measured afterwards. In addition, the concentrations of pro-inflammatory indicators related to LPS in the blood serum were also determined. Heat stress was more severe in period I, during which a higher (P < 0.0001) temperature humidity index (THI) was recorded compared to period II. The increase of DCAD by supplementing NaHCO3 and K2CO3 enhanced (P < 0.01) the levels of endotoxin in the urine during period I, whilst lowered (P < 0.01) the endotoxin concentration in plasma during period II. Raising DCAD also decreased (P < 0.01) the levels of lipopolysaccharide binding protein (LBP) and serum amyloid A (SAA) in the serum during period I. The interaction between treatment and period occurred for the concentrations of LPS across four biofluids and a few inflammatory mediators in the serum. Increasing DCAD differently altered the LPS concentrations in rumen liquid (P < 0.01) and milk (P < 0.01), as well as the interleukin (IL)-2 level in serum (P < 0.05) dependent on the period. This study implies that elevating DCAD modified the distribution of LPS endotoxin across different biofluids and affected inflammation response in Holstein cows under heat stress, and it necessitates further investigations to reveal the underlying mechanisms.