Despite therapeutic advances, mortality rates for neonatal meningitis have remained the same over the last two decades. Addressing this requires better understanding of how the disease is caused at a cellular and molecular level. Here we see the re-distribution of the protein beta-catenin (blue) in brain endothelial cells after infection by the bacteria Escherichia coli K1. This bacterium (the small, rod-like cells seen in the grayscale image) has been shown to cause neonatal meningitis.
Led by principal investigator Prasadarao Nemani, PhD, researchers in the Microbial Pathogenesis Research Lab at Children’s Hospital Los Angeles generated this image to better understand the cellular and molecular events that occur when these bacteria pass through the blood-brain barrier as occurs in cases of neonatal meningitis. Beta-catenin helps coordinate adhesion between cells and, in cases of neonatal meningitis, the adhesion between brain endothelial cells is disrupted, leading to brain edema or swelling where fluid accumulates in the brain.
“This helped us identify that re-distribution of beta-catenin helps the bacteria invade the brain endothelium and may serve as a critical step in causing neonatal meningitis,” say Subramanian Krishnan, post-doctoral fellow at Children’s Hospital Los Angeles, who was first author on the study published in Cellular Microbiology.
Image courtesy of Subramanian Krishnan, Prasadarao Nemani, PhD, and Esteban Fernandez, PhD, The Saban Research Institute, Children’s Hospital Los Angeles.