**4. Iron uptake systems of uropathogenic** *Escherichia coli*

Urinary tract has limited iron. However, UPEC are able to produce small iron chelator molecules, known as siderophores, to scavenge ferric iron (Fe3+) in the host. The most prominent ones are yersiniabactin, salmochelin, and aerobactin [48, 49]. The yersiniabactin and its receptor, FyuA, are encoded in a PAI [50, 51]. It has also been reported that for efficient biofilm formation by UPEC, FyuA is required [52]. UPEC also secretes another important hydroxamate siderophore called aerobactin. This is produced from the condensation of two lysine and a citrate molecules. During UPEC invasion, the bacterium secretes salmochelin. Its outer membrane siderophore receptor (IroN) transports different catechol siderophores, including N-(2,3-dihydroxybenzoy)-L-serine and enterochelin also called enterobactin [53]. Enterobactin has less solubility and stability than

*Virulence Factors of Uropathogenic* Escherichia coli *DOI: http://dx.doi.org/10.5772/intechopen.99891*

#### **Figure 1.**

*UPEC-associated fitness and virulence. Adapted from the work by Servin [64].*

aerobactin [54–56] but has higher iron affinity than aerobactin in aqueous [55, 57]. UPEC also uses enterobactin for Fe3+ scavenging in the urinary tract [9]. However, enterobactin can be inactivated by the host proteins such as serum albumin and siderocalin thereby preventing its uptake [58]. UPEC overcomes this instability by modifying the enterobactin to salmochelin by glucosylation through the enzymatic action of glucosyltransferase and prevents it from being recognized by the host proteins [9]. Also, UPEC has another iron acquisition system called haemin uptake system consisting of Ton-B dependent receptor (ChuA) and heavy metal associated (*Hma*) receptor that takes part in direct upregulation of haem receptors from free iron during UPEC infection. This system has also been reported to play significant role in the formation of biofilm [59–61]. The expression of ChuA is controlled by other regulatory proteins. It has been reported that the production of ChuA is triggered as RfaH increases [62]. However, Hma does not depend on ChuA and it is controlled by Tyr-126. Both Hma and ChuA are associated with haem uptake for optimal kidney utilization [63]. **Figure 1** shows the diagram of UPEC-associated fitness and virulence factors.
