Prior infections appear to shield enteric neurons, preventing these key components of the body’s ‘second brain’ from dying off when future pathogens strike.

But there may be an upside to enteric infection. A new study finds that mice infected with bacteria or parasites develop a unique form of tolerance quite unlike the textbook immune response. The research, published in Cell, describes how gut macrophages respond to prior insult by shielding enteric neurons, preventing them from dying off when future pathogens strike. These findings may ultimately have clinical implications for conditions such as irritable bowel syndrome, which have been linked to the runaway death of intestinal neurons.

«We’re describing a sort of innate memory that persists after the primary infection is gone,» says Rockefeller’s Daniel Mucida. «This tolerance does not exist to kill future pathogens, but to deal with the damage that infection causes — preserving the number of neurons in the intestine.»

Neuronal cause of death

Known as the body’s «second brain,» the enteric nervous system is houses the largest depot of neurons and glia outside of the brain itself. The GI tract’s own nervous system exists more or less autonomously, without significant input from the brain. It controls the movement of nutrients and waste by fiat, coordinating local fluid exchange and blood flow with authority not seen anywhere else in the peripheral nervous system.

If enough of those neurons die, the GI tract spirals out of control.

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