Figure 3.

Suppression of intestinal antimicrobial activity by modifying bacterial virulence and iron stores. (A) Normally high-affinity, iron-binding proteins, such as Tf, prevent free iron (Fe) being made available to microbes to limit their growth and dissemination into exogenous tissues. Concentrations of catecholamines (NE; E) increase in the intestinal lumen following traumatic stress. (B) The catechol moiety acts as a magnet to mediate sequestration of iron from Tf and shift the balance to an iron-rich environment. Quarum-sensing mechanisms signals the bacteria to increase the expression of bacterial virulence factors, siderophores, which facilitate the internalization of iron liberated from Tf by NE/E. Ultimately, iron use allows for greater microbial growth and an increased capacity of the bacteria to adhere and possibly disseminate to distal sites to cause infection.