Enhancing host defense against Brucella: The immune effect exerted by anti-OMP16 monoclonal antibody

Brucellosis is an important zoonotic infection caused by the Gram-negative, facultative intracellular bacterium, Brucella. The disease is widespread and prevalent throughout the world, posing a serious threat to human health, with over 500,000 new cases each year. Combination antibiotic therapy is the current treatment for brucellosis, but owing to its intracellular survival capability, the effectiveness of antibiotics is significantly reduced, Monoclonal antibodies (mAbs) are a promising class of biodrugs with a wide range of applications in the clinical treatment of disease. Brucella outer membrane protein 16 (OMP16) is a crucial virulence factor of Brucella for maintaining outer membrane integrity and survival; thus, it is a potential immunotherapy target. In this study, we demonstrated that an anti-Brucella OMP16 IgM-type monoclonal antibody, B7, was able to bind to and agglutinate Brucella abortus A19, and activate the complement system to kill the bacteria. We found that B7 could enhance phagocytosis and killing against Brucella by activating complement in RAW264.7 macrophages, upregulate intracellular nitric oxide and reactive oxygen species levels to enhance cellular resistance to infection, and induce the expression of relevant immunomodulatory cytokines. The antibody's immunoprotective effect was confirmed in a mouse model of Brucella infection. Our study demonstrated that B7 mAb has the potential to provide a new immunotherapeutic approach for the clinical treatment of brucellosis and for related vaccine and drug research.