Fig. 8. Model demonstrating the interplay between NE and SerpinA3N during infection.
a Citrobacter rodentium infection induces the recruitment of neutrophils. In response to inflammatory triggers NE is released. SerpinA3N is produced and secreted by infected IECs to protect from NE-induced damage. In mild disease (e.g. C57 mice), the balance is in favour of the inhibitor (i.e. excess free SerpinA3N). b In severe disease (e.g. C3H mice), there is insufficient SerpinA3N to neutralise excess luminal NE activity, which results in IEC cell death (grey cell with fragmented membrane and nuclei). c The balance can be pushed in favour of the inhibitor in C3H mice using engineered C. rodentium to deliver SerpinA3N.