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The effects of grain-induced subacute ruminal acidosis (SARA) in lactating dairy cows on free ruminal lipopolysaccharide (LPS) and indicators of inflammation were determined. Four mid lactation dairy cows were divided into 2 groups of 2 cows and used in a repeated switchover design. During each period, SARA was induced in 2 animals for 5 subsequent days by replacing 25% of their total mixed ration (dry matter basis) with a concentrate made of 50% wheat and 50% barley. The other 2 cows acted as controls and were fed a total mixed ration diet in which 44% of dry matter was concentrate. On average, inducing SARA did not affect milk composition, increased the duration of rumen pH below 5.6 from 187 to 309 min/d, and increased free ruminal LPS concentration from 24,547 endotoxin units (EU)/mL to 128,825 EU/mL. Averaged across treatments, milk fat yield and milk protein yield were 0.66 and 1.00kg/d, respectively. Rumen pH and milk fat data suggest that control cows also experienced ruminal acidosis, albeit a milder form of this disease than SARA cows. Serum LPS concentration in both control and SARA cows was less than the detection limit of <0.01 EU/mL for the assay. Induction of SARA elevated serum amyloid A concentration from 286.8 to 498.8μg/mL, but did not affect other markers of inflammation including haptoglobin, fibrinogen, serum copper, or white blood cells. These results suggest that grain-induced SARA in mid lactation dairy cows increases the lysis of gram-negative bacteria and activates an inflammatory response.

Background/Aims: Subacute ruminal acidosis (SARA) is a common disease in high-producing lactating cows. Rumenitis is the initial insult of SARA and is associated with the high concentrations of histamine produced in the rumen of dairy cows during SARA. However, the exact mechanism remains unclear. The objective of the current study is to investigate whether histamine induces inflammation of rumen epithelial cells and the underlying mechanism of this process. Methods: Bovine rumen epithelial cells were cultured and treated with different concentrations of histamine and pyrrolidine dithiocarbamate (PDTC, an NF-κB inhibitor) cultured in different pH medium (pH 7.2 or 5.5). qRT-PCR, Western-blotting, ELISA and immunocytofluorescence were used to evaluate whether histamine activated the NF-κB pathway and inflammatory cytokines. Results: The results showed that histamine significantly increased the activity of IKK β and the phosphorylation levels of IκB α, as well as upregulated the mRNA and protein expression levels of NF-κB p65 in the rumen epithelial cells cultured in neutral (pH=7.2) and acidic (pH=5.5) medium. Furthermore, histamine treatment also significantly increased the transcriptional activity of NF-κB p65. High expression and transcriptional activity of NF-κB p65 significantly increased the mRNA expressions and concentrations of inflammatory cytokines, tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6) and interleukin 1 beta (IL-1β), thereby inducing the inflammatory response in bovine rumen epithelial cells. However, inhibition of NF-κB p65 by PDTC significantly decreased the expressions and concentrations of the inflammatory cytokines induced by histamine in the rumen epithelial cells cultured in the neutral and acidic medium. Conclusion: The present data indicate that histamine induces the inflammatory response of bovine rumen epithelial cells through the NF-κB pathway.

The effects of a grain-based subacute ruminal acidosis (SARA) challenge on translocation of lipopolysaccharide (LPS) into the peripheral circulation, acute phase proteins in blood and milk, feed intake, milk production and composition, and blood metabolites were determined in 8 lactating Holstein cows. Between wk 1 and 5 of 2 successive 6-wk periods, cows received a total mixed ration ad libitum with a forage to concentrate (F:C) ratio of 50:50. In wk 6 of both periods, the SARA challenge was conducted by replacing 21% of the dry matter of the total mixed ration with pellets containing 50% wheat and 50% barley. Rumen pH was monitored continuously using indwelling pH probes in 4 rumen cannulated cows. Rumen fluid samples were collected 15min before feed delivery and at 2, 4, 6, 12, 14, 16, 18, and 24h after feed delivery for 2 d during wk 5 (control) and wk 6 (SARA). Peripheral blood samples were collected using jugular catheters 15min before feeding and at 6 and 12h after feeding at the same days of the rumen fluid collections. The SARA challenge significantly reduced average daily pH from 6.17 to 5.97 and increased the duration of rumen pH below pH 5.6 from 118 to 279 min/d. The challenge reduced dry matter intake (16.5 vs. 19kg/d), milk yield (28.3 vs. 31.6kg/d), and milk fat (2.93 vs. 3.30%, 0.85 vs. 0.97kg/d), and tended to increase milk protein percentage (3.42 vs. 3.29%), without affecting milk protein yield (1.00 vs. 0.98kg/d). The challenge also increased the concentration of free LPS in rumen fluid from 28,184 to 107,152 endotoxin units (EU)/mL. This was accompanied by an increase in LPS in peripheral blood plasma (0.52 vs. <0.05 EU/mL) with a peak at 12h after feeding (0.81 EU/mL). Concentrations of the acute phase proteins serum amyloid A, haptoglobin, and LPS-binding protein (LBP) in peripheral blood as well as LBP concentration in milk increased (438.5 vs. 167.4, 475.6 vs. 0, 53.1 vs. 18.2, and 6.94 vs. 3.02μg/mL, respectively) during SARA. The increase in LBP in combination with the increase in LPS in peripheral blood provides additional evidence of translocation of LPS. Results suggest that the grain-based SARA challenge resulted in translocation of LPS into the peripheral circulation, and that this translocation triggered a systemic inflammatory response.

Subacute ruminal acidosis (SARA) is a common metabolic disease in ruminants. In the early stage of SARA, ruminants do not exhibit obvious clinical symptoms. However, SARA often leads to local inflammatory diseases such as laminitis, mastitis, endometritis and hepatitis. The mechanism by which SARA leads to inflammatory diseases is largely unknown. The gut microbiota is the totality of bacteria, viruses and fungi inhabiting the gastrointestinal tract. Studies have found that the gut microbiota is not only crucial to gastrointestinal health but also involved in a variety of disease processes, including metabolic diseases, autoimmune diseases, tumors and inflammatory diseases. Studies have shown that intestinal bacteria and their metabolites can migrate to extraintestinal distal organs, such as the lung, liver and brain, through endogenous pathways, leading to related diseases. Combined with the literature, we believe that the dysbiosis of the rumen microbiota, the destruction of the rumen barrier and the dysbiosis of liver function in the pathogenesis of SARA lead to the entry of rumen bacteria and/or metabolites into the body through blood or lymphatic circulation and place the body in the “chronic low-grade” inflammatory state. Meanwhile, rumen bacteria and/or their metabolites can also migrate to the mammary gland, uterus and other organs, leading to the occurrence of related inflammatory diseases. The aim of this review is to describe the mechanism by which SARA causes inflammatory diseases to obtain a more comprehensive and profound understanding of SARA and its related inflammatory diseases. Meanwhile, it is also of great significance for the joint prevention and control of diseases.

The demand for economic benefits has led to an increase in the proportion of high-concentrate (HC) feed in the ruminant diet, resulting in an increased incidence of subacute ruminal acidosis (SARA). During SARA, a high concentration of lipopolysaccharide (LPS) translocated in the rumen induces a systemic inflammatory response. Inflammatory diseases, such as endometritis and mastitis, are often associated with SARA; however, in sheep, the mechanism of the effect of SARA on the endometrium has rarely been reported. Therefore, the aim of this study was to investigate, for the first time, the influence of LPS translocation on endometrial tight junctions (TJs) during SARA in sheep. The results showed that LPS and TNFα levels in the ruminal fluid, serum, and endometrial tissue supernatant during SARA increased, transcription levels of TLR4, NFκB, and TNFα in the endometrium increased, the protein expression level of claudin-1 in the endometrium increased, and the protein expression level of occludin decreased. 17β-estradiol (E2) inhibits claudin-1 protein expression and promotes occludin expression, and progesterone (P4) promotes claudin-1 protein expression and inhibits occludin protein expression. E2 and P4 regulate claudin-1 and occludin protein expression through their receptor pathways. Here, we found that LPS hindered the regulatory effect of E2 and P4 on endometrial TJs by inhibiting their receptor expression. The results of this study indicate that HC feeding can cause SARA-induced LPS translocation in sheep, increase susceptibility to systemic inflammation, induce the endometrial inflammatory response, and cause endometrial epithelial TJ damage directly and/or by obstructing E2 and P4 function. LPS translocation caused by SARA has also been suggested to induce an endometrial inflammatory response, resulting in endometrial epithelial barrier damage and physiological dysfunction, which seriously affects ruminant production. Therefore, this study provides new evidence that SARA is a potential factor that induces systemic inflammation in ruminants. It provides theoretical support for research on the prevention of endometritis in ruminants.

Background Subacute ruminal acidosis (SARA) is a metabolic disease in high-producing dairy cattle, and is accompanied by rumenitis. However, the mechanism of rumenitis remains unclear. Therefore, the aim of this study was to investigate the molecular mechanism of rumenitis in dairy cows with SARA. Results The results showed that SARA cows displayed high concentrations of ruminal volatile fatty acids, lactic acid and lipopolysaccharide (LPS). Furthermore, the blood concentrations of LPS and acute phase proteins haptoglobin, serum amyloid-A, and LPS binding protein were significantly higher in SARA cows than in control cows. Importantly, the phosphorylation levels of nuclear factor-kappaB (NF-κB) p65, inhibitor of NF-κB (IκB), c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase 1/2 (ERK1/2) were significantly higher in the rumen epithelium of SARA cows than those of control cows. The ruminal mRNA and protein levels of NF-κB- and mitogen-activated protein kinase (MAPK)s -regulated inflammatory cytokines, tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and interleukin 1β (IL-1β), were markedly higher in SARA cows than in control cows. Similarly, serum concentrations of TNF-α and IL-6 were also significantly higher in SARA cows. Conclusions These results indicate that SARA results in high concentration of ruminal LPS, which over activates the NF-κB and MAPKs inflammatory pathways and then significantly increases the expression and synthesis of pro-inflammation cytokines in the rumen epithelium, thereby partly inducing rumenitis.

The rumen metabolic environment from either SARA susceptible (S) or unsusceptible (U) cows, was hypothesized to alter the fermentative capacity and bacterial community composition. This was evaluated in vitro through exposure for a period of 24 h of the microbial inoculum of three donor cows to sterile ruminal supernatant obtained from a subset of 15 out of a group of 38 early lactating dairy cows which were either SARA S ( n  = 8) or U ( n  = 7) cows at pH 5.8 and 6.8. Compared to exposure to sterile supernatant from S cows, microbiota exposed to sterile supernatant from U cows produced more total volatile fatty acids, irrespective of the in vitro pH (6.8 or 5.8). Specifically, branched-chain volatile fatty acids (BCVFA), such as isobutyrate and total BCVFA are elevated/tended to be elevated in incubations with the sterile supernatant from U cows. Net lactate accumulation in incubations with U cows’ supernatant at pH 6.8 was higher than with S cows’ supernatant. Nevertheless, a lower relative abundance of Firmicutes , uncultured Ruminococcaceae , Lachnospiraceae_UCG-008 , and Anaerovoracaceae Mogibacterium , as well as a higher relative abundance of Prevotella was observed after incubation with sterile supernatant from SARA S cows as compared with SARA U cows.

Subacute ruminal acidosis (SARA) has emerged as a prevalent digestive disorder that significantly affects the overall health of ruminants, with notable links to various inflammatory diseases. Throughout the progression of SARA, elevated lipopolysaccharide (LPS) levels in the rumen play a crucial role in initiating the innate immune response. In this review, we evaluate the recent insights into the pathways associated with SARA-induced inflammatory responses, with a specific focus on LPS. It is important to recognize the variation in the immune response activation potential of LPS derived from different bacterial sources. This variability aligns with the widespread detection of LPS in the rumens of ruminants with SARA. Nonetheless, trained immunity is expected to become a novel strategy for the prevention and control of SARA. This mechanism offers a rapid response to secondary stimuli, including LPS, effectively preventing inflammation. Ultimately, this review establishes a comprehensive system integrating SARA, LPS, and trained immunity. Through this integrated approach, we aim to provide innovative solutions to the challenges associated with SARA.

Subacute ruminal acidosis (SARA) is usually characterized by abnormal and intermittent drops in rumen pH. Nevertheless, high individual animal variability in rumen pH and the difference in measurement methods for pH data acquisition decrease the sensitivity and accuracy of pH indicators for detecting SARA in ruminants. The aim of this study was to refine rumen pH indicators in long-term SARA based on individual dairy cow reticulo-rumen pH kinetics. Animal performances and rumen parameters were studied weekly in order to validate SARA syndrome and rumen pH was continuously measured using reticulo-rumen sensors. In total, 11 primiparous dairy cows were consecutively fed two different diets for 12 successive weeks: a control diet as low-starch diet (LSD; 13% starch for 4 weeks in period 1), an acidotic diet as high-starch diet (HSD; 32% starch for 4 weeks in period 2), and again the LSD diet (3 weeks in period 3). There was a 1-week dietary transition between LSD and HSD. Commonly used absolute SARA pH indicators such as daily average, area under the curve (AUC) and time spent below pH<5.8 and pH<6 were processed from absolute (raw) daily kinetics. Then signal processing was applied to raw pH values in order to calculate relative pH indicators by filtering and normalizing data to remove inter-individual variability, sensor drift and sensor noise. Normalized AUC, times spent below NpH<−0.3 and NpH<−0.5, NpH range and NpH standard deviation were calculated. Those relative pH indicators were compared with commonly used pH indicators to assess their ability to detect SARA. This syndrome induced by HSD was confirmed by consistent expected changes in milk quality, dry matter intake and acetate : propionate ratio in the rumen, whereas the ruminal concentration of lipopolysaccharide was increased. Commonly used pH SARA indicators were not able to discriminate SARA syndrome due to high animal variability and sensor drift and noise, whereas relative pH indicators developed in this study appeared more relevant for SARA detection as assessed by receiver operating characteristic tests. This work shows that absolute pH kinetics should be corrected for drift, noise and animal variability to produce relative pH indicators that are more robust for SARA detection. These relative pH indicators could be more relevant for identifying affected animals in a herd and also for comparing SARA risk among studies.

Background The prevalence of subacute ruminal acidosis (SARA) in dairy cows is high with large impact on economy and welfare. Its current field diagnosis is based on point ruminal pH measurements by oral probe or rumenocentesis. These techniques are invasive and inaccurate, and better markers for the diagnosis of SARA are needed. The goal of this study was to evaluate clinical signs of SARA and to investigate the use of blood, faecal and urinary parameters as indicators of SARA. Six lactating, rumen cannulated, Danish Holstein cows were used in a cross-over study with three periods. The first and second periods included two cows on control diet and two cows on nutritional SARA challenge. The third period only included two cows on SARA challenge. Control diet was a conventional total mixed ration [45.5% dry matter (DM), 17.8% crude protein, 43.8% neutral detergent fibre, and 22.5% acid detergent fibre (DM basis)]. SARA challenge was conducted by substituting control diet with grain pellets (50% wheat/barley) over 3 days to reach 40% grain in the diet. Ruminal pH was measured continuously. Blood samples were collected once daily at 7 h after feeding. Samples of faeces and urine were collected at feeding, and at 7 and 12 h after feeding. Blood samples were analysed for pCO2, pO2, pH, electrolytes, lactate, glucose, packed cell volume (PCV), and total plasma protein concentration. Milk composition, ruminal VFA, and pH of faeces and urine were measured. Results SARA was associated with decreased ( P  < 0.05) minimum ruminal, faecal and urinary pH. Daily times and areas of ruminal pH below 5.8, and 5.6 were increased to levels representative for SARA. Significant differences were detected in milk composition and ruminal VFAs. Blood calcium concentration was decreased ( P  < 0.05), and pCO 2 tended to be increased ( P  = 0.10). Significant differences were not detected in other parameters. Conclusions SARA challenge was associated with changes in faecal and urinary pH, blood calcium concentration and pCO 2 . These may be helpful as indicators of SARA. However changes were small, and diurnal variations were present. None of these parameters are able to stand alone as indicators of SARA.