Michael Cremin

Neonatal Enteric Infection Disrupts the Microbiota-Gut-Brain Axis Through Pattern Recognition Receptors and Altered Neuroimmune Signaling

This study shows that neonatal EPEC infection disrupts the microbiota-gut-brain axis via NOD1 signaling, leading to long-term neuroimmune and behavioral deficits, and identifies probiotic muropeptides as potential therapeutics.

Tac1 Deficiency Reduces the Severity of Enteric Bacterial Infection

This study shows that Tac1 deficiency reduces C. rodentium infection severity by lowering inflammation and immune cell recruitment.

The sympathetic nervous system enhances host immune responses to enteric bacterial pathogens.

This study shows that the sympathetic nervous system enhances immune responses to enteric bacterial infections by modulating IFN{gamma} production in CD4+ T-cells via alpha-adrenergic receptors.

Inhibition of acute lung inflammation by a neuroimmune circuit induced by vagal nerve stimulation.

This study identifies a neuroimmune circuit activated by afferent vagus nerve stimulation that reduces acute lung inflammation through epinephrine and β2-adrenergic receptor signaling.

Substance P receptor signaling contributes to host maladaptive responses during enteric bacterial infection.

This study shows that blocking Substance P receptor signaling reduces inflammation and prevents maladaptive responses during enteric bacterial infection without affecting host protection.