Innate immune lectins kill bacteria expressing blood group antigen

Stowell, S. et al. Nat. Med. 2010; 16, 295-301

Speaker: Nai-Chi Yeh (葉乃綺)                                     Time: 14:00~15:00, Dec. 8, 2010

Commentator: Dr. Trai-Ming Yeh (葉才明教授)          Place: Room 601

Abstract:

There are many pathogens in the environment, some of which express ABO (H) blood group antigens. Adaptive immunity cannot generate antibodies against these pathogens bearing blood group-like structure, whereas innate immunity is required to eliminate them. Recent studies suggest that members of the innate immune lectins, including galectin family, have several diverse functions in inflammation or immunological activity.^[1] In this study, the authors analyzed public data from the Consortium for Functional Glycomics, and discovered that human galectin-4 (Gal-4) and galectin-8 (Gal-8) can recognize human blood group A and B antigens, but do not bind blood group O (H) antigens. They demonstrated that these two galectins specifically recognize human blood group B (BGB⁺)-expressing Escherichia coli by C-terminal domains.^[2] In addition, treatment of Gal-4 and Gal-8 not only results in rapid loss of mobile capability of BGB⁺ E. coli, but also directly kills it by altering membrane integrity in vivo and in vitro. Unlike other innate immune lectins, such as mannose-binding proteins, Gal-4 and Gal-8 kill BGB⁺ E. coli without a requirement for the help of complement.^[3] Thus, these results demonstrate that innate immune lectins, Gal-4 and Gal-8, have ability to specifically defense the infection of pathogens which express blood group-like antigens.

References:

1.      Vasta, G.R. Roles of galectins in infection. Nat. Rev. Microbiol. 2009; 7, 424-438.

2.      Liu, F.T. et al. A sweet target for innate immunity. Nat. Med. 2010; 16, 263-264.

3.      Thiel, S. et al. A second serine protease associated with mannan-binding lectin that activates complement. Nature 1997; 386, 506–510.