Intact Cell Ultrastructure Is Sufficient for the Intestinal Protective Activity of Canine-Derived Lactobacillus acidophilus Against Dextran Sulfate Sodium-Induced Colitis

Chronic inflammatory enteropathy is common and clinically challenging in dogs. Probiotics are explored as dietary adjuncts, but how inactivation methods affect strain performance remains unclear. This study compared viable, heat-killed, electron beam-inactivated (3 kGy), and cell-free supernatant (CFS) preparations of canine-origin Lactobacillus acidophilus L1 in a DSS-induced mouse colitis model. Heat-killed L1 retained intact ultrastructure and matched viable cells in attenuating disease activity and colonic injury; electron beam inactivation disrupted the cell surface and produced poorer repair than heat-killed L1 but was superior in maintaining body weight. All treatments lowered DAI versus the model (p < 0.001). Colon length and Zo-1/Occludin mRNA expression were highest in viable and heat-killed groups, which also had the lowest splenic and hepatic indices (p < 0.01). IL-17A fell further in viable and heat-killed groups (p < 0.01); IL-10 rose only in these two groups (p < 0.05). Cecal SCFAs were elevated in DSS and CFS groups despite reduced Dubosiella. Heat-killed bacteria had the lowest cecal SCFAs but the highest MCT1/SMCT1 expression (p < 0.05) and unchanged MCT4 expression, potentially suggesting enhanced epithelial SCFA uptake, although reduced microbial production cannot be excluded. These results indicate that intact bacterial ultrastructure is sufficient for the intestinal protective activity of L. acidophilus L1 in a prophylactic model, and support heat-killed L1 as a promising prophylactic paraprobiotic ingredient for canine gastrointestinal health.