Influence of dietary Saccharomyces cerevisiae fermentation product on markers of inflammation and cartilage metabolism in young exercising horses challenged with intra-articular lipopolysaccharide.

The objective was to evaluate dietary Saccharomyces cerevisiae fermentation product (SCFP) on joint inflammation and cartilage metabolism in exercising yearlings challenged with intra-articular lipopolysaccharide (LPS), hypothesizing dietary SCFP (TruEquine^®C, Diamond V Mills, Inc.) would ameliorate joint inflammation and increase cartilage metabolism. Thirty Quarter Horse yearlings were stratified by bodyweight (BW), age, sex, and randomly assigned to dietary treatments (n = 10/treatment): control (0), 46, or 92 mg/kg BW/d SCFP. Treatments were top-dressed to 1% BW/d concentrate void of added microbials. Horses were stalled (3.6 m × 7.3 m), offered ad libitum Coastal bermudagrass hay, and exercised 30 min/d, 5 d/wk. On days 0, 21, 42, and 56, wither height, hip height, heart girth, body length, body condition scores (BCS), and BW were recorded. On day 46, one radial carpal joint received 0.8 mL of a 0.5 ng LPS solution or sterile lactated Ringer's solution (LRS) in the contralateral joint. Synovial fluid was collected pre- (0) and 6, 12, 24, and 336 hours post-injection and analyzed for prostaglandin E₂ (PGE₂), carboxypropeptide of type II collagen (CPII), and collagenase cleavage neopeptide (C2C) via commercial ELISA, and chemokines (CCL2, and CCL11) and cytokines (TNF $\alpha$ and IL-10) via multiplex platform. Rectal temperature (RT), heart rate (HR), respiration rate (RR), and carpal circumference (CC) were recorded prior to arthrocentesis. Data were analyzed using PROC MIXED of SAS. By day 56, growth parameters increased (P < 0.01), BCS did not change (P = 0.39), and BW had a treatment × d interaction (P = 0.02) where control tended to be heavier than 92 mg/kg BW on day 56 (P = 0.07). Clinical parameters (RT, HR, RR, CC) were uninfluenced by diet (P ≥ 0.29) but varied over time (P ≤ 0.03). Treatments did not influence cartilage metabolism (CPII, C2C, and CPII:C2C) (P ≥ 0.46) or logPGE₂, logCCL2, CCL11, or logIL-10 (P ≥ 0.23). There was a treatment × h interaction for CCL11 (P = 0.04) where control was greater than SCFP groups at h 6. LogIL-10 had a treatment × h interaction where 46 mg/kg BW was lower than control and 92 mg/kg BW at h 12 (P = 0.05). There was a main effect of treatment for TNF $\alpha$ (P = 0.04) where 92 mg/kg BW was lower than 46 mg/kg BW and tended to be lower than control. Results indicate that SCFP didn't influence cartilage metabolism or PGE₂, though SCFP may ameliorate inflammatory cytokines and chemokines following an acute, intra-articular insult.