Twenty-four individually housed Holstein bulls (395 ± 7.3 kg BW and 252 ± 3.1 d age) were exposed to a 2 × 2 factorial design (meal vs. pellet and with vs. without straw) to evaluate the effect of concentrate form and provision of straw in finishing diets. Concentrate and straw consumption were recorded monthly, and behavior by scan sampling biweekly. Bulls were slaughtered after 64 d. Rumen and liver lesions were recorded and tissue samples were collected. Data were analyzed using an ANOVA. Straw supplementation increased (P < 0.01) percentage of rumination observations (9.4 vs. 3.1 ± 1.02%), and decreased (P < 0.01) oral non-nutritive behaviors (0.74 vs. 1.68 ± 0.12 times/15 min) relative to bulls not provided straw. Provision of straw increased rumen pH, but the magnitude was greater when meal was provided compared with pellet (interaction P < 0.05). When straw was not supplemented, all rumens had papillae fusion, whereas only 16.7% of bulls fed pellet and straw had papillae fusions (P < 0.05). In the rumen straw provision numerically increased expression of free fatty acid receptor 2 (stimulates PYY and serotonin secretion, P = 0.06), α-2C adrenergic receptor (modulates immune reactions and behavior, P = 0.09), and increased occludin and claudin-4 (tight junction proteins, P < 0.05), along with IL-1β, TNFα (pro-inflammatory cytokines, P < 0.01) and toll-like receptor-4 (P < 0.01); moreover, it also numerically increased β-defensin1 (antimicrobial peptide, P = 0.10), and intestinal alkaline phosphatase (P = 0.10), and increased CASP3 (pro-apoptotic gene, P < 0.05) and numerically increase SPC25 (proliferative marker, P = 0.06). Pellet decreased rumen gene expression of α-2C adrenergic receptor (P < 0.05) and increased occludin (P = 0.06) and monocarboxylate transporter 1 (P < 0.05). Bulls without straw had increased expression of IL-1β in the cecum. In conclusion, the lack of straw supplementation in bulls fed high-concentrate diets modifies behavior, affects rumen macroscopic morphology, and expression of epithelial genes related to inflammation.