The study shows that pieces of cell walls from Streptococcus pneumoniae bacteria "hijack" a protein on the lining of the blood vessel wall and use it to slip out of the bloodstream and into the brain and heart. A report on this study appears in the November 1 issue of the Journal of Immunology. These findings explain why blood stream infection with S. pneumoniae commonly leads to temporary impairment of heart function, and they suggest a way to prevent that from occurring, according to Elaine Tuomanen, M.D., chair of the St. Jude Department of Infectious Diseases. S. pneumoniae is a leading cause of pneumonia, sepsis (a potentially life-threatening bloodstream infection) and meningitis (inflammation of the membranes surrounding the brain and spinal cord).
The St. Jude team found that pieces of cell wall from S. pneumoniae that escape from the bloodstream enter neurons (brain cells). In a previous report published in the July issue of Infection and Immunity, St. Jude researchers reported that in the mouse model, cell wall fragments damaged neurons in the part of the brain called the hippocampus. Tuomanen is senior author of both reports.
In the current study, the researchers showed how the cell wall fragments escape the bloodstream and enter cells. Specifically, they demonstrated that pieces of the bacterial cell wall bind to the vascular endothelium (inner surface of the blood vessel) by hooking onto a protein called platelet activating factor receptor (PAFr). Platelet activating factor (PAF) is an immune system signaling molecule that activates
Source:St. Jude Children's Research Hospital