Dietary probiotic form modulates broiler gut microbiota indices and expression of gut barrier genes including essential components for gut homeostasis.

The probiotic form (PF) type and its dietary administration in combination or not with avilamycin (AV) were investigated for their effects on broiler gut microbiota and expression of genes relevant for gut barrier and gut homeostasis. Depending on PF type (i.e. no addition, viable, inactivated) and AV addition (no/yes), 450 one-day-old Cobb male broilers were allocated in 6 treatments (CON, CON + A, ViP, ViP + A, InP and InP + A) according to a 3 × 2 factorial arrangement with 5 replicates of 15 broilers each for 42 days. Significant interactions (P  ≤ 0.05) between PF and AV administration were shown for the ileal mucosa-associated bacteria, the caecal digesta Lactobacillus spp., the molar ratio of the sum of valeric, hexanoic and heptanoic acids and the gene expressions of ileal and caecal IgA and ileal claudin 1. Avilamycin suppressed ileal digesta Lactobacillus spp. (P  < 0.001) and caecal digesta Clostridium perfringens subgroup (P  = 0.018) and modulated the intestinal fermentation intensity and pattern. The viable PF had the higher levels of ileal digesta Bacteroides spp. (P  = 0.021) and caecal digesta Lactobacillus spp. (P  = 0.038) compared with the other two PF. Probiotic form modulated the microbial metabolic activity in the ileum and caeca with the viable PF being the most noteworthy in terms of effects regarded as beneficial. Furthermore, the viable PF resulted in reduced expression of caecal Toll-like receptors TLR2B (P  = 0.026) and TLR4 (P  = 0.011) and transcription factor NFΚΒ1 (P  = 0.002), which could be considered as essential for limiting inflammation and preserving gut homeostasis. In conclusion, under non-challenge conditions, probiotic function was shown to depend on PF type and to a lesser degree on co-administration with AV. The importance of probiotic viability for the beneficial modulation of important gut components towards a reduced state of physiological inflammation has been highlighted.