Virulence factors of uropathogenic Escherichia coli L. Emo ˝dy *, M. Kere ´nyi, G. Nagy Department of Medical Microbiology and Immunology, University Medical School of Pe ´cs, Szigeti ut 12, H-7624 Pe ´cs, Hungary Abstract Virulence factors of Escherichia coli are of two main types; those produced on the surface of the cell and those produced within the cell and then exported to the site of action. Those on the surface include different sorts of fimbriae that have a role in adhesion to the surface of host cells but may also have additional roles such as tissue invasion, biofilm formation or cytokine induction. The activities of cell wall components are discussed and several exported virulence factors are described that have anti host cell activities. Others virulence factors enable the bacteria to grow in an environment of iron restriction. # 2003 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved. Keywords: Virulence factors; Fimbriae; Adhesion; Cytotoxicity 1. Introduction Escherichia coli is by far the most common pathogen isolated from urinary tract infections (UTI), and fre- quently originates from the patients’ own intestinal flora. However, only some members of the normal flora elicit an infection in persons without local or general predisposing conditions to UTI. E. coli clones present in the large intestine are not equally able to initiate and maintain the infectious process in the urinary tract. Special components or products, called virulence fac- tors, enable E. coli cells to colonise selectively the mucosal uro-epithelium, evoke an inflammatory reac- tion and eventually proceed from the lower urinary tract to the renal cavities and tissues. 2. Surface virulence factors Surface virulence factors of the pathogen (Table 1) include various adhesins mainly of fimbrial nature. Type 1 fimbriae (called also type 1 pili) may promote bacterial adhesion, invasion and growth as a biofilm [1  /3]. These fimbriae recognise manno-oligosaccharides naturally presented on glycoprotein molecules of the host cell surface. Allelic variations of the FimH adhesin subunit determine the fine sugar specificity of these fimbriae. Pathoadaptive mutations play an important role in tissue tropism and infectivity of type 1 fimbriated E. coli [1  /6]. P fimbrial lectins recognise a digalactoside component of the P blood group antigen also abundantly positioned on the surface of urinary epithelial cells [7]. Molecular contact between the mucosal surface and the pathogen induces lipopolysaccharide (LPS) independent trans- membrane signalling and epithelial cell activation. Concomitant interleukin (IL-6 and IL-8) production promotes the development of local inflammation [8,9]. S fimbriae and F1C fimbriae have also been impli- cated in the process of UTI. They both show binding efficiency to epithelial and endothelial cell lines derived from the lower human urinary tract and kidney [10,11]. Thin aggregative fimbriae [12], also called curli, are expressed on about 50% of urinary E. coli isolates. They are optimally expressed at ambient temperature and in this way they may promote colonisation of the perineal area initiating a subsequent UTI [13]. All the above fimbriae producing species are also able to bind to various matrix components facilitating tissue invasion by the pathogen [14]. Minor subunits posi- tioned proximal to the adhesin subunit are responsible for this function in the case of P and S fimbriae. Flagellar motility contributes to the virulence of Proteus mirabilis in ascending UTI [15]. Mouse studies using a pyelonephritis model suggest that swarm cell * Corresponding author. Tel.:  /36-72-536-252; fax:  /36-72-536- 253. E-mail address: levente.emody@aok.pte.hu (L. Emo ˝ dy). International Journal of Antimicrobial Agents 22 (2003) S29  /S33 www.ischemo.org 0924-8579/03/$30 # 2003 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved. doi:10.1016/S0924-8579(03)00236-X