Wednesday, March 9, 2016

Holy Wicked Twist Batman

Maternal bacterial infections trigger abnormal proliferation of neurons in fetal brain

"The finding was unexpected because in children and adults pneumococcal infections can lead to meningitis and the death of neurons," said the study's corresponding author Elaine Tuomanen, M.D., chair of the St. Jude Department of Infectious Diseases. "This study in a mouse model of the bacterial infection found that prenatally the opposite is true. The evidence suggests maternal infections cause a signaling event that leads to the proliferation and reorganization of neurons in the developing brain that is defective in some way, maybe due to overcrowding."
Researchers showed for the first time that pieces of the bacterial cell wall crossed the placenta and traveled to the fetal brain, triggering proliferation of immature neurons. Evidence suggested the proliferation was sparked by a previously unrecognized pathway that involves the innate immune system and a protein that regulates gene expression.
The proliferation resulted in a 50 percent increase in neurons in a region of the developing brain that becomes the cortex, which is responsible for thought, action and other higher functions.
Investigators also reported that mice exposed to bacterial cell wall early in fetal development later performed below average on measures of memory and cognitive functioning. Researchers also found evidence that treatment of maternal infection by the antibiotic ampicillin, which destroys bacteria and sends pieces of the cell wall into the bloodstream, led to a similar neuronal increase.
Tuomanen said the results raise questions about which class of antibiotics should be used to treat bacterial infections during pregnancy. "This study suggests widely used antibiotics like ampicillin that cause bacteria to burst and release cell wall may lead to changes in the developing brain," she said. "Such changes did not occur in mice treated with antibiotics like clindamycin that kill without releasing cell wall.