Passive immunotherapy with specific IgG fraction against autolysin: Analogous protectivity in the MRSA infection with antibiotic therapy.

Staphylococcus aureus is a leading infectious cause of life-threatening diseases in human beings, with no effective vaccine available to date against this bacterium. Treatment of methicillin-resistant S. aureus (MRSA) infections has become increasingly difficult because of the emergence of multidrug-resistant isolates. Immunotherapy represents a potential approach to prevent S. aureus-related infections. Autolysin is one of the virulence factors, which controls the growth, cell lysis, daughter-cell separation, and biofilm formation. Our study focused on passive immunization against MRSA infection. Herein, rabbit polyclonal IgG was produced following the preparation of r-autolysin. Specificity of IgG against r-autolysin was investigated by ELISA and western blotting assays. IgG fraction was prepared using sulfate ammonium precipitation, and the ability of antiserum to promote phagocytosis of bacteria was assessed by opsonophagocytosis assay. Then, passive immunization of mice was carried out with polyclonal IgG fraction and, mice were sacrificed three days after challenge and their kidneys, liver, and spleen were collected. Results exhibited that the passive immunization with rabbit polyclonal anti-IgG fraction tremendously improved survival rates of mice challenged by S. aureus as well as vancomycin treatment compared with the negative control groups. In addition, a remarkable decrease in bacterial numbers was observed in mice treated with rabbit polyclonal anti-IgG. Importantly, our findings demonstrated that passive immunotherapy and antibiotic therapy lead to decreased histopathological damage in mice infected by S. aureus as compared with control groups. Our results suggested that the passive immunization may result in the introduction of excellent strategies to control infections caused by MRSA, like antibiotic therapy.
(Copyright © 2018 European Federation of Immunological Societies. Published by Elsevier B.V. All rights reserved.)