**1. Introduction**

Infertility is currently a highly prevalent disease, defined by the failure to achieve a successful pregnancy after 12 months or more of appropriate, unprotected intercourse or therapeutic

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donor insemination [1]. Approximately 50% of infertility cases are attributed to the male [2, 3] due to conditions such as varicocele, cryptorchidism, obstructive problems, hormonal disor‐ ders, ejaculatory dysfunction as well as infectious causes classified under male genital tract infection (MGTI).

**3. Effect of** *E. coli* **on human spermatozoa is induced through seminal** 

One way *E. coli* induces damage in spermatozoa is by mediating seminal leukocyte activation. The increased presence of leukocytes in semen, known as leukocytospermia, is defined by a

cytokines, which are usually released by leukocytes during the inflammatory response, are able to decrease sperm motility by themselves [5, 18, 19]. This damaging effect seems to be mediated by polymorphonuclear (PMN) leukocytes instead of by other leukocytes such as lymphocytes or monocytes [20]. The decrease in sperm quality is also mediated by reactive oxygen species (ROS) released by PMN after bacteria‐induced activation, with *E. coli* being able to induce a higher response of increased ROS production than other bacteria [9]. Other consequences of ROS released by leukocytes are lipid peroxidation, which affects sperm plasma membrane [21, 22], and early induction of sperm capacitation, which should normally

The direct effect of *E. coli* on sperm was demonstrated through *in vitro* studies performed by directly incubating both cells. It has been demonstrated by several authors that *E. coli* com‐ ing into contact with spermatozoa causes decreased sperm motility [7, 24–26]. The decrease in sperm motility due to *E. coli* has been attributed for many years to an agglutinating effect on sperm [27]. Sperm agglutination can be caused by bacterial type 1 and P fimbriae; specifi‐ cally, the type 1 fimbriae of *E. coli* cause a pattern of head‐head type agglutination because they bind mannose residues in the head region of sperm. Instead, type P fimbriae of *E. coli* cause a head‐tail agglutination pattern because they bind gal‐gal receptors present along the

Electron microscopy has revealed that this bacterium causes damage primarily in the head of spermatozoa, such as rupture of the plasma membrane, vesicle formation and rupture of the

Consistent with the plasma membrane damages observed, another report showed that *E. coli* per se causes phosphatidylserine translocation, a cell death indicator [9]. From the point of view of sperm cell death, it was observed that *E. coli* endotoxins such as lipopolysaccha‐ ride (LPS), peptidoglycan and porins produce loss of sperm viability [30]. Moreover, it has been shown that LPS and porins cause sperm DNA fragmentation [31]. The effects of these endotoxins are mediated by the toll‐like receptor (TLR)‐2 and TLR‐4, both present in sperm. After TLR‐2 and TLR‐4 stimulation, sperm damage highlighting DNA fragmentation can be

Another direct effect of *E. coli* is at the level of mitochondrial membrane potential (ΔΨm). The *in vitro* observation that contact with *E. coli* decreases the ΔΨm together with the motility in

leukocytes per ml of semen [17]. Proinflammatory

http://dx.doi.org/10.5772/intechopen.68312

73

Effect of Uropathogenic *Escherichia coli* on Human Sperm Function and Male Fertility

**leukocytes**

sperm [28].

observed [32].

concentration equal to or greater than 1 x 10<sup>6</sup>

occur later in the female reproductive tract [23].

inner and outer membranes of the acrosome [29].

**4.** *E. coli* **directly affects human sperm function**

MGTI accounts for 15% of male infertility cases [4]. MGTIs are an important problem in male reproductive health because they cause negative changes in semen parameters [5]. A consequence of MGTI is the inflammatory response evidenced by leukocytospermia, where a treatment with antibiotics and anti‐inflammatory drugs may be helpful to try to recover the patient's fertilizing potential [6]. Principal causes of MGTI are bacteria such as *Staphylococcus epidermidis*, *Streptococcus viridans*, *Staphylococcus aureus* and *Escherichia coli* (*E. coli*), which have a negative effect on the fertilizing potential of a man and are strongly associated with MGTI [7, 8]. However, *E. coli has* been shown to exert greater damaging effects on human sperma‐ tozoa [7, 9–11].

*E. coli* is the causal agent in 65–80% of cases of chronic bacterial prostatis [12], and these bacte‐ ria have been isolated from semen in 69% of the patients with this pathology [13]. Moreover, *E. coli* causes diverse MGTIs such as urethritis, epididymitis and orchitis, and it is the most frequently isolated bacterium [4].

With this background, this chapter discusses the negative effect of *E. coli on* sperm quality and male fertility. The chapter will be developed by first addressing the uropathogenic *E. coli strains* associated with male infertility. Then, the evidence of the *in vitro* effects of *E. coli on* the male gamete will be analyzed. Evidences will be described, obtained after *in vitro* co‐incu‐ bation of normal human spermatozoa with *E. coli and* with polymorphonuclear leukocytes, emulating infection. Next, the effects of *E. coli* on human sperm functions observed by direct incubation of spermatozoa with bacteria and without leukocytes will be discussed. Also, evi‐ dence of the effects of the metabolic and soluble products of *E. coli* on human sperm function will be analyzed. To complete the picture of the evidence of the effects of this bacterium on male fertility, some studies on animal models will be reviewed.
