Research ArticleHost-Pathogen Interactions

Carbohydrate-dependent B cell activation by fucose-binding bacterial lectins

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Sci. Signal.  05 Mar 2019:
Vol. 12, Issue 571, eaao7194
DOI: 10.1126/scisignal.aao7194

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Sweet B cell activation

Burkholderia and Pseudomonas species of proteobacteria secrete carbohydrate-binding proteins called lectins, enabling adhesion to host tissues and biofilm formation, which can lead to opportunistic infections. Wilhelm et al. showed that fucose-binding bacterial lectins bound to and activated mouse B cells in vitro, which depended on the B cell antigen receptor and the kinase Syk. In vivo, these lectins induced a strong but transient immune response characterized by increased numbers of B cells and myeloid cells in the spleen. These data suggest that bacterial lectins may act like antigens to hijack B cell signaling and stimulate rapid immune responses, which may pose a risk to immunocompromised individuals.

Abstract

Bacterial lectins are typically multivalent and bind noncovalently to specific carbohydrates on host tissues to facilitate bacterial adhesion. Here, we analyzed the effects of two fucose-binding lectins, BambL from Burkholderia ambifaria and LecB from Pseudomonas aeruginosa, on specific signaling pathways in B cells. We found that these bacterial lectins induced B cell activation, which, in vitro, was dependent on the cell surface expression of the B cell antigen receptor (BCR) and its co-receptor CD19, as well as on spleen tyrosine kinase (Syk) activity. The resulting release of intracellular Ca2+ was followed by an increase in the cell surface abundance of the activation marker CD86, augmented cytokine secretion, and subsequent cell death, replicating all of the events that are observed in vitro upon canonical and antigen-mediated B cell activation. Moreover, injection of BambL in mice resulted in a substantial, BCR-independent loss of B cells in the bone marrow with simultaneous, transient enlargement of the spleen (splenomegaly), as well as an increase in the numbers of splenic B cells and myeloid cells. Together, these data suggest that bacterial lectins can initiate polyclonal activation of B cells through their sole capacity to bind to fucose.

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