Rumen-derived lipopolysaccharide provoked inflammatory injury in the liver of dairy cows fed a high-concentrate diet

Abstract

Rumen-derived lipopolysaccharide (LPS) is translocated from the rumen into the bloodstream when subacute ruminal acidosis (SARA) occurs following long-term feeding with a high-concentrate (HC) diet in dairy cows. The objective of this study was to investigate the mechanism of inflammatory responses in the liver caused by HC diet feeding. We found that SARA was induced in dairy cows when rumen pH below 5.6 lasted for at least 3 h/d with HC diet feeding. Also, the LPS levels in the portal and hepatic veins were increased significantly and hepatocytes were impaired as well as the liver function was inhibited during SARA condition. Meanwhile, the mRNA expression of immune genes including TNF receptor associated factor 6 (TRAF6), nuclear factor-kappa B (NF-κB), p38 mitogen-activated protein kinase (MAPK), extracellular regulated protein kinases (ERK) MAPK, Interleukin-1 (IL-1) and serum amyloid A (SAA) in the liver were significantly increased in SARA cows. Moreover, the phosphorylation level of NF-κB p65 and p38 MAPK proteins in the liver and the concentration of Tumor Necrosis Factor (TNF-α), Interleukin-1β (IL-1β) and Interleukin-6 (IL-6) in peripheral blood were obviously increased under SARA condition. In conclusion, the inflammatory injury in the liver caused by LPS that traveled from the digestive tract to the liver through the portal vein after feeding with a HC diet.

Impacts of Time-Fed Concentrate-Based Diets on Plasma Metabolites, Rumen Histology, and mRNA Expression of Hepatic Enzymes of Wethers

“…In situations where these animals are not appropriately transitioned to concentrate-based diets, ruminal acidosis can occur [1]. Ruminal acidosis can negatively affect the integrity and barrier function of the rumen epithelium by increasing parakeratosis, vacuolation, and cell degeneration [2,3] The loss of barrier function in the rumen epithelium can lead to the translocation of bacteria, and its endotoxins (lipopolysaccharides), from the rumen into the systemic circulation and result in a hepatic acute phase response [4]. The acute phase response is caused by systemic inflammation and is characterized by the increase or decrease in acute phase reactants.…”

Effects of activated charcoal and zeolite on serum lipopolysaccharides and some inflammatory biomarkers levels in experimentally induced subacute ruminal acidosis in lambs

“…Also, in agreement with the present study, Dong et al [29] reported that when the rumen pH of goats decreased to less than 5.8, plasma LPS value in the high-grain group was not significantly different from the low-grain groups. Elevated serum LPS levels as a result of SARA induction in cattle [9,14,33] are also expected in sheep. A possible reason for this discrepancy might be the insufficient sensitivity of LPS measurement methods in the studies on sheep and goats [12].…”

“…In other words, oral consumption of activated charcoal and zeolite in lambs with SARA resulted in significant reductions in serum LPS concentrations. There are enough understandings on pivotal role of LPS in causing multiple adverse sequels following SARA in ruminants [14,15,33]. It has been shown that as toxin binders, certain clay minerals such as bentonite and zeolite are able to trap free rumen bacterial toxins [23] and mycotoxins [34,35] in cattle.…”

“…LPS or endotoxin could be translocated into the blood, resulting in many complications such as inflammatory responses, ruminal stasis, tissue poor blood supply, and weakness [13]. Various studies have shown the adverse sequels of increased rumen and blood LPS, including lameness [9], liver changes [14], and induced inflammatory responses [12] in SARA. Inflammatory responses have been surveyed in SARA [15][16][17].…”

“…APPs including serum amyloid A, haptoglobin, fibrinogen, and C reactive protein (CRP) are useful indicators for detecting inflammatory processes in ruminants [4,18,19]. Contrary to the acute ruminal lactic acidosis whose pathogenicity is mainly related to increased blood D and L-lactic acid values [4], and also oxidative stress [20], numerous investigations of SARA have shown that a major part of SARA pathogenicity is attributed to LPS [12][13][14]. On the other hand, few attempts have been made to inhibit LPS absorption in SARA or acute ruminal acidosis [21,22].…”