52 Influence of Saccharomyces cerevisiae CNCM I-1077 on the intestinal environment, gut permeability, and markers of systemic inflammation in horses fed a high starch diet

Abstract

Probiotics may balance the hindgut environment and relieve systemic inflammation in horses fed high starch concentrates to meet energy requirements. Therefore, 30 mature Quarter Horse geldings (545 ± 58 kg BW) were used in a randomized complete design for 32-d to test the hypothesis that supplemental live Saccharomyces cerevisiae CNCM I-1077 (SC; Levucell® SC Advantage) stabilizes the intestinal environment, reduces gut permeability, and decreases inflammation when horses are fed a high starch diet. Horses were stratified by BW, age, and body condition score (BCS) and randomly assigned treatments consisting of either a concentrate formulated with 2g starch • kg BW−1 • meal−1 (CON, n = 15) or the same concentrate top-dressed with 25 g/d SC(TRT, n = 15) containing 20 billion cfu. Horses were fed individually in stalls (3 × 3 m) every 12 h. Between meals, horses were housed in adjacent dry lots with ad libitum access to Coastal bermudagrass hay and water. On d 0 and 32, BW and BCS were recorded and blood samples were collected immediately before feeding (h 0) and at h 2, 8, 16, and 24 post meal. Samples were analyzed for serum D-lactate using a colorimetric assay, chemokine (CCL2) and cytokine (TNFα) concentrations were measured using a multiplex platform, and whole blood 16s rRNA sequencing was performedusing Illumina MiSeq. Fecal samples were obtained on d 0, 16, and 32 via rectal palpation before the morning meal and at h 8, 16, and 24 post meal. Fecal pH was determined using a portable pH meter and fecal starch was measured via concentration analysis. Data were analyzed using PROC MIXED of SAS v9.4. Non-normal data (CCL2) were log-transformed. From d 0 to 32 BW increased (P ≤ 0.01), independent of treatment, with no change in BCS (P = 0.97). Fecal starch was undetectable indicating nearly complete digestion of dietary starch regardless of treatment. On d 0, fecal pH declined to h 16 (P ≤ 0.01) in both groups and returned to baseline by h 24 post meal. At h 0, CON had lower fecal pH on d 32 than d 0 (P ≤ 0.01). D-lactate peaked at h 8 on d 0, and CON was greater (P ≤ 0.01) than TRT. On d 32, D-lactate tended to be higher in TRT (P = 0.10) at 16 h post meal compared with CON. LogCCL2 and TNFα declined (P ≤ 0.02) across treatments to d 32. Fold change of percent reads from d 0 in bacterial 16s rRNA was not different between treatment groups. A high starch diet initially reduced fecal pH and increased BW but after 32 d, there was no difference in intestinal inflammation or gut permeability, regardless of SC supplementation.