Abstract

Background Salmonella typhimurium is a pathogen that causes gastroenteritis in humans and animals. Amuc_1100 (hereafter called Amuc), the outer membrane protein of Akkermansia muciniphila , alleviates metabolic disorders and maintains immune homeostasis. Objective This study was conducted to determine whether there is a protective effect of Amuc administration. Methods Male 6-wk-old C57BL6J mice were randomly allocated into 4 groups: CON (control), Amuc (gavaged with Amuc, 100 μg/d for 14 d), ST (oral administration of 1.0 × 10 6 CFU S . typhimurium on day 7), and ST + Amuc (Amuc supplementation for 14 d, S . typhimurium administration on day 7). Serum and tissue samples were collected 14 d after treatment. Histological damage, inflammatory cell infiltration, apoptosis, and protein levels of genes associated with inflammation and antioxidant stress were analyzed. Data were analyzed by 2-way ANOVA and Duncan’s multiple comparisons using SPSS software. Results The ST group mice had 17.1% lower body weight, 1.3–3.6-fold greater organ index (organ weight/body weight for organs including the liver and spleen), 10-fold greater liver damage score, and 3.4–10.1-fold enhanced aspartate transaminase, alanine transaminase, and myeloperoxidase activities, and malondialdehyde and hydrogen peroxide concentrations compared with controls ( P < 0.05). The S . typhimurium -induced abnormalities were prevented by Amuc supplementation. Furthermore, the ST + Amuc group mice had 1.44–1.89-fold lower mRNA levels of proinflammatory cytokines (interleukin [Il] 6, Il1b , and tumor necrosis factor-α) and chemokines (chemokine ligand [Ccl]2, Ccl3 , and Ccl8 ) and 27.1%–68.5% lower levels of inflammation-related proteins in the liver than ST group mice ( P < 0.05). Conclusions Amuc treatment prevents S . typhimurium -induced liver damage partly through the toll-like receptor (TLR)2/TLR4/myeloid differentiation factor 88 and nuclear factor-κB signaling as well as nuclear fact