B-Cell Activation Is Increased Following Exposure to Freshwater Algal Toxin Microcystin and Anabaenopeptin-B

Bethany Garcia-Cortez, “B-Cell Activation Is Increased Following Exposure to Freshwater Algal Toxin Microcystin and Anabaenopeptin-B” 

Mentor: Michael Laiosa, Public Health, Public Health (Joseph J. Zilber School of) 

Poster #3 

Cyanobacteria are naturally occurring in freshwater lakes, however, in recent years, due to climate change and excess nutrient runoff, there’s been an increase in uncontrolled growth of these organisms leading to harmful algal blooms. When a cyanobacterial harmful algal bloom (CHAB) forms, there is a high potential of toxin release in the lake that could be harmful to people and the environment. The only algal toxin that is regulated by the EPA is one called microcystin, but this toxin is the tip of the iceberg of what we know exists in our freshwater ecosystems. Therefore, the purpose of this study is to better understand potential human health impacts of these non-regulated toxins, beginning with a toxin referred to as anabaenopeptin. Our testing of the health impacts of these toxins was focused on immune cell activation, and for these studies, we utilized a B cell line maintained in the laboratory using sterile technique. This required maintaining the health of the cells using microscopy and other lab instrumentation. We grew the cells in nutrient-filled media and split them every two days to optimize health. We first conducted an experiment with both microcystin and anabaenopeptin-B in a controlled environment, to define the effects of these toxins on the B cell antigen receptor signaling threshold. We found that B-cells exposed to anabaenopeptin-B and microcystin were overly activated compared to the control B-cells. In the context of human cells, if these results occurred in people, it could potentially reduce the threshold necessary for normal B cells to become activated. The consequences of such a state might be higher levels of inflammation and potentially elevated risk of developing an autoimmune disease.