Abstract
Subacute Ruminal Acidosis (SARA) is a disorder in cattle which can lead to chronic inflammation in the rumen epithelium, known as rumenitis. Butyrate has been shown to attenuate some of the detrimental effects of inflammatory gastroenteral disorders but the molecular mechanisms mediated by butyrate have not been defined. The objective of this study was to define the inflammatory-related genomic changes responsible for the beneficial effects of butyrate. Experimentally, 16 fistulated dairy cows at mid-lactation were fed a SARA-inducing (45% non-fiber carbohydrate) diet beginning 2 days before the beginning of treatment and continuing throughout the experiment. Cows were then evenly divided into treatment groups where a carrier with (n = 8) or without (n = 8) supplemental butyrate (2.5% initial DM intake) was deposited into the rumen daily for 7 days. The minimum rumen pH was higher in cows with supplemental butyrate (4.96±0.09 to 5.20±0.05, p = 0.040), but mean pH, maximum pH and the duration for which rumen pH was below 5.6 was unaffected. Free plasma Lipopolysaccharide (LPS) concentration was unaffected by treatment as was the concentration of Serum Amyloid A (SAA), although the LPS Binding Protein (LBP) concentration was increased by the addition of butyrate to the rumen (6.91±0.29 to 7.93±0.29 µg mL-1, p = 0.024). Of the rumen Short Chain Fatty Acids (SCFA) tested, only butyrate showed a pronounced treatment effect, rising from 8.60±0.94 to 21.60±0.94 mM (p≤0.0001). Plasma Beta-Hydroxybutyrate (BHBA) concentration also increased (799.50±265.24 to 3261.63±265.24 µM, p≤0.001). Butyrate infusion did not affect milk parameters (total fat, lactose, total protein and LOS); however, when related to dry matter intake, milk production efficiency was increased (p = 0.035). Microarray and qRT-PCR analyses of rumen papillae biopsies collected on day 7 found that butyrate administration affected (p≤0.05) the expression of genes involved in Non-Specific Host Defense (NSHD), Remodeling or adaptation (RM) and Immune Response (IR). Of the 49 genes tested by qRT-PCR, 9 (LCN2, MMP1, MUC16, GPX2, CSTA, FUT1, SERPINE2, BCAM, RAC3) were upregulated, 20 (MTOR, AKIRIN2, NFKBIZ, NFKB2, ACVR2A, LAMB1, FRS2, PPARD, LBP, NEDD4L, SGK1, DEDD2, MAP3K8, PARD6B, PLIN2, ADA, HPGD, FMO5, BMP6, TCHH) were downregulated and 20 were unchanged due to butyrate administration in the proximal gastrointestinal tract. These results demonstrate the potential protective effect and molecular mechanisms involved in a novel butyrate treatment for inflammatory gastrointestinal conditions.
Highlights
Subacute Ruminal Acidosis (SARA) is a chronic pathological inflammatory condition of the rumen, affecting approximately 20% of all dairy cattle in North America (Garrett et al, 1999)
Despite the fact that the transmigration of microbes across the rumen wall has been documented in cases of SARA, we have shown that this effect involves the immune system, the extent of immune system stimulation is limited to local events and is not detectable systemically (Dionissopoulos et al, 2012a; 2012b)
Since the effects of SARA on rumen physiological dynamics have been reported (Keunen et al, 2002; Penner et al, 2007), we sought to determine the effects of butyrate treatment on milk production, milk components, pH, Short Chain Fatty Acids (SCFA), SCFA metabolism, the effects on Non-Specific Host Defense (NSHD) and evidence for an Immune Response (IR)
Summary
SARA is a chronic pathological inflammatory condition of the rumen, affecting approximately 20% of all dairy cattle in North America (Garrett et al, 1999). Due primarily to the microbial fermentation to SCFA of soluble starch of high grain diets, SARA can lead to liver abscesses, laminitis and acute inflammation of the rumen epithelium (Kleen et al, 2003; Plaizier et al, 2008). SARA does this by causing a sloughing of the rumen epithelium, compromising epithelial integrity (Steele et al, 2011a). We have shown that adaptation to a SARA diet takes place within three weeks (Steele et al, 2011a) and previous experiments have shown that one of the principle methods by which the rumen adapts to an acidotic diet is by increasing papillae size and the total absorptive surface area of the rumen (Gabel et al, 2002), by increasing cellular turnover and an overall increase in total epithelial cell number (Goodlad, 1981)
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