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MAE4, an eLtaS monoclonal antibody, blocks Staphylococcus aureus virulence.


ABSTRACT: Staphylococcus aureus causes a wide range of infectious diseases. Treatment of these infections has become increasingly difficult due to the widespread emergence of antibiotic-resistant strains; therefore, it is essential to explore effective alternatives to antibiotics. A secreted protein of S. aureus, known as eLtaS, is an extracellular protein released from the bacterial membrane protein, LtaS. However, the role of eLtaS in S. aureus pathogenesis remains largely unknown. Here we show eLtaS dramatically aggravates S. aureus infection by binding to C3b and then inhibiting the phagocytosis of C3b-deposited S. aureus. Furthermore, we developed a monoclonal antibody against eLtaS, MAE4, which neutralizes the activity of eLtaS and blocks staphylococcal evasion of phagocytosis. Consequently, MAE4 is capable of protecting mice from lethal S. aureus infection. Our findings reveal that targeting of eLtaS by MAE4 is a potential therapeutic strategy for the treatment of infectious diseases caused by S. aureus.

SUBMITTER: Liu Y 

PROVIDER: S-EPMC4657049 | biostudies-literature | 2015 Nov

REPOSITORIES: biostudies-literature

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MAE4, an eLtaS monoclonal antibody, blocks Staphylococcus aureus virulence.

Liu Yu Y   Feng Jiannan J   Lu Qiang Q   Zhang Xin X   Gao Yaping Y   Yan Jun J   Mu Chunhua C   Hei Yan Y   Lv Ming M   Han Gencheng G   Chen Guojiang G   Jin Peng P   Hu Weiguo W   Shen Beifen B   Yang Guang G  

Scientific reports 20151124


Staphylococcus aureus causes a wide range of infectious diseases. Treatment of these infections has become increasingly difficult due to the widespread emergence of antibiotic-resistant strains; therefore, it is essential to explore effective alternatives to antibiotics. A secreted protein of S. aureus, known as eLtaS, is an extracellular protein released from the bacterial membrane protein, LtaS. However, the role of eLtaS in S. aureus pathogenesis remains largely unknown. Here we show eLtaS dr  ...[more]

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