**1. Introduction**

The most commonly living microorganism of the human gastrointestinal tract and also the most common causative agent of bacterial urinary tract infection is *E. coli* [1]. Though they remain in a good relationship with their hosts, they might appear as a subject of consideration in immunocompromised hosts. This common inhabitant of the gastrointestinal tract usually remains in a symbiotic relationship with the host and plays a role in maintaining the homeostasis of the intestinal tract. Though most of the strains of *E. coli* are harmless, some serotypes can cause food poisoning. *E. coli* present in the normal human microbiota produces

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

vitamin K2 . Strains of *E coli*, however, obtaining ability to colonize inside the urinary tract and to make themselves safe from the host immune system, become uropathogenic *E. coli*. UPEC causes >80% of UTI [2]. Urinary tract infections are very common, and approximately 10% of people [3] and half of all women (at least one time) become infected throughout their life. According to a study, more than 100,000 patients in the United States are hospitalized annually due to urinary tract infections [4], and in the year 2011, 400,000 patients were hospitalized, and the estimated cost was about 2.8 billion USD [5]. Infections can occur in both upper and lower urinary tracts. Lower urinary tract infection is known as cystitis, and in the case of upper urinary tract infection, it is called pyelonephritis. Without distinction of site, in order to cause infection, the causative agent must at first dodge the host's immune system and colonize in the urinary tract [6]. Several different virulent factors are needed for the bacterial population to cause infections [7]; for instance, pathogenic strains of *E. coli* express adherence factors which form pili or fimbriae of different types for their attachment in the sites where they usually do not live [7]; these are structural virulence factors and predominantly include P fimbriae and type 1 fimbriae [1]. Fimbrial adhesins such as PapG and CsgA are virulence factors that facilitate the attachment of *E. coli* [8]. In animal models, type 1 fimbriae aggrandize the chance survival of *E. coli* [9]. Beside these, UPEC can impair host immune system by a variety of ways [10], such as toxins and iron acquisition systems, and these are called secreted virulence factors. The production of these virulence factors by UPEC may cause an inflammatory response which makes a possible pathway for UTI symptoms [1]. However, both the host and the uropathogenic *E. coli* strain have different roles in the establishment and colonization process in the urinary tract [11]. Here in this chapter, different types of important virulence factors of uropathogenic *E. coli* will be discussed.

surface of bacteria that recognize specific compounds usually carbohydrates of the target host cells [11]. Pili are the short form of fimbriae and might be used interchangeably with fimbriae. Fimbriae consist of oligomeric pilin proteins. These proteins are arranged in such a manner that they form a helical cylindrical structure and are both thinner and shorter than flagellum. These proteinaceous structures are expressed in uropathogenic strains of *E. coli* and are considered as virulence factors [11]. Most of the receptors for these fimbriae are carbohydrates. They include type 1 fimbriae, P fimbriae, and thin aggregative fimbriae [16]. Many bacterial pathogens can produce an array of these adhesins, and often inhibition of a single adhesin may cost enough to a bacterium to lose its virulence. Functions of pili or fimbriae are not limited only to adhesion and can help in many other crucial pathways for the microbe to survive and evade the immune system of the host. Evolution of different types of adhesins plays a role in tissue tropism.

Virulence Factors of Uropathogenic *E. coli* http://dx.doi.org/10.5772/intechopen.79557 9

In gram-negative bacteria like UPEC, adhesins are unveiled by chaperone-usher-assisted pathway. This pathway involves two proteins, one is a periplasmic chaperone, and the other is a protein called usher. Usher act as the base of the structure, and the function of chaperone is folding and recruitment of the subunits [17, 18]. In absence of the chaperone, pilin proteins are degraded and misfolded and thus cannot be assembled in the form of a mature pilus. On the other hand, usher helps to mature the fimbriae and its transportation through the outer assuring integrity of the outer membrane. The constituents of usher proteins are an N-terminal domain (NTD), 24-stranded beta-barrel channel, a plug domain, and two C-terminal domains (CTD). In uropathogenic *E. coli* strains, chaperone-usher family fimbriae are more abundant.

In 99% of *E. coli* strains, genes to encode type 1 fimbriae are present [19], and during urinary tract infections, they damage urinary tract cells by mediating an increased inflammation [20]. In order to enter into the host cells of the urinary tract, type 1 fimbriae play a great role. Type 1 fimbriae are remarkably versatile virulence factors of UPEC that can stabilize the attachment of the bacteria to different type of cells throughout the urinary tract. Though in Bowman's capsules and glomerulus their binding sites could not be identified, a strong affinity of type 1 fimbriae was found in proximal tubules and vessel walls. In the bladder, they bind strongly to muscular layers and moderately to vessel walls. Receptors for type 1 fimbriae were also found in the distal tubules and collecting ducts. They can also induce their binding to the surface of macrophages [9]. These fimbriae recognize uroplakin from bladder epithelial cells and mannoside-containing host proteins. Unlike many other important types of adhesins, these are encoded by the bacterial backbone DNA [21] and are mainly composed of FimA proteins along with FimF, FimG, and FimH [17]. FimA proteins are most in number but are not pivotal for virulence. Among other subunits of type 1 fimbriae, allelic variations of FimH determine the sugar specificity and deletion of *fimH* results in less amount of colonization in mouse models of ascending UTI, and colonization could be restored by expression of plasmid with *fimH* gene [20]. FimH alone or in association with LPS can stimulate toll-like receptor 4 (TLR4) to initiate particular signaling cascade that may activate the humoral immune response. Many studies revealed that expression of type 1 fimbriae results in virulence and loss of expression results in loss of expression but their presence cannot be correlated with UTI as normal fecal strains also have equally expressed type 1 fimbriae [22]. However, type 1 fimbriae-mediated attachment is a crucial stage for cystitis. Adhesins of

**2.1. Type 1 fimbriae**

these fimbriae are mannose sensitive.

In Gram-negative and some Gram-positive bacteria, virulence genes are allocated in particular segments (about 10–200 kilo bases in size) of their genome which have different G + C content than the other parts of the genome that are termed as pathogenicity islands. They are present in the virulent strains but present rarely in the nonpathogenic strains of the same species. These sequences can be transferred horizontally from species to species [12]. Pathogenicity islands encode virulence factors such as adherence factors, toxins, and iron acquisition systems which are important virulence factors of UPEC.
