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

Area of Science:

• Immunology
• Microbiology
• Molecular Biology

Background:

• Bacterial lectins mediate adhesion to host tissues by binding specific carbohydrates.
• Fucose-binding lectins are implicated in bacterial pathogenesis.
• B cell activation is crucial for adaptive immunity and host defense.

Purpose of the Study:

• To investigate the effects of fucose-binding bacterial lectins BambL and LecB on B cell signaling and activation.
• To elucidate the molecular mechanisms underlying lectin-induced B cell responses.
• To assess the in vivo consequences of bacterial lectin administration on B cell populations.

Main Methods:

• In vitro analysis of B cell activation markers, intracellular calcium release, and cytokine secretion upon lectin treatment.
• Assessment of B cell antigen receptor (BCR), CD19, and spleen tyrosine kinase (Syk) involvement in lectin-induced signaling.
• In vivo studies involving BambL injection in mice to evaluate effects on B cell populations in bone marrow and spleen.

Main Results:

• Bacterial lectins BambL and LecB induced B cell activation in vitro, dependent on BCR, CD19, and Syk.
• Lectin-mediated B cell activation led to calcium release, CD86 expression, cytokine secretion, and cell death.
• In vivo BambL injection caused B cell depletion in bone marrow, splenomegaly, and altered splenic B and myeloid cell populations.

Conclusions:

• Fucose-binding bacterial lectins can act as potent polyclonal activators of B cells.
• Bacterial lectins can initiate B cell responses independently of antigen recognition.
• These findings highlight a novel mechanism of bacterial immune modulation through direct B cell activation.