• Bifidobacteria;
  • dextran sulfate sodium-induced colitis;
  • Lactobacilli;
  • Toll-like receptor 2 monoclonal antibody;
  • Toll-like receptor 4 monoclonal antibody;
  • ulcerative colitis


Background and Aim:  The accurate pathogenesis of ulcerative colitis (UC) is not yet well understood. Recently, Toll-like receptor 2 (TLR2), TLR4 and gut microbial flora have been proved as playing important roles in the process of UC. This study was to evaluate the effect of TLR2 and TLR4 monoclonal antibodies on gut microbial flora in dextran sulfate sodium (DSS)-induced colitis in a mouse model.

Methods:  We evaluated the effects of the TLR2 and TLR4 monoclonal antibodies on the development of DSS-induced colitis. Clinical symptoms were evaluated by the disease activity index (DAI), while tissue samples were evaluated by histological scoring (HS). Meanwhile, the mucosal mRNA expressions of TLR2, TLR4, interferon-γ (IFN-γ), interleukin-4 (IL-4) and IL-17 were analyzed by Realtime polymerase chain reaction (PCR). The mucosal protein TRAF6, TAB1, P-IKK, P-P38α mitogen-activated protein kinase (MAPL) and c-jun expressions of the TLR2 and TLR4 signaling pathways were analyzed using Western blot. The mucosal nuclear factor kappa B (NF-κB) was analyzed using electrophoretic mobility shift assay. Fecal samples were obtained directly from the cecum for microbiological studies.

Results:  Expressions of TLR2 and TLR4 in colonic epithelial cells on DSS-induced colitis were much higher than normal ones. After the treatment with TLR2mAb and TLR4mAb, DAI and HS were decreased significantly. The UC model group showed a conspicuous increase of Escherichia coli and decreases of Lactobacillus spp. and Bifidobacterium spp. After being treated with TLR2mAb or/and TLR4mAb, Lactobacillus spp. and Bifidobacterium spp. increased to the normal level.

Conclusions:  TLR2mAb and TLR4mAb can suppress the development of DSS-induced colitis and increase counts of Lactobacilli and Bifidobacteria.