While the underlying mechanism governing this phenotype requires further study, it is likely that the compromised antimicrobial activity of MPO-deficient neutrophils7,21 undermined successful killing and elimination of local microbial invaders, resulting in unresolved infection and sustained stimulation of local epithelium, which triggers overproduction of neutrophil chemoattractants, chemokines or leukotriene B4.22 Thus, MPO-deficient mice had more PMNs recruited to the submucosal area and subsequently migrated into the lumen, promoting neutrophilic inflammation in the intestine. Here, MPO is linked to infection.