Activation of Leukocytes

Infection of the genital tract is often observed as an asymptomatic subclinical inflammation [55, 56] with up to 80% of leukocytospermic semen samples showing no visual detection of microbial infection [26]. Following infiltration of infectious agents into the genital tract, the initial immune reaction is the increase in seminal leukocytes [15]. This inflammatory process aimed at killing the microorganisms results in the increase in leukocyte-produced ROS from the activated WBC's [11]. The infiltration and activation of these excess PMNL can cause excessively high concentrations of ROS which greatly exceed the required level for normal physiological functions. This elevation results in OS being initiated which produces a damaging prooxidant load I 36 I . Irrelevant of the concentration of leukocytes in semen, the presence of these WBC have been shown to be associated with OS and impairment in the quality of semen and sperm parameters such as concentration and morphology [7].

Two pathways are found in response to the activation of seminal leukocytes during infection. The first is the increase of NADPH through the hexose monophosphate shunt [32, 57]. The second route is the generation of high concentrations of ROS produced by a respiratory burst which acts as a protective mechanism following the infection [1, 32]. The result is the antioxidants in the cell being consumed. This oxidative burst is from the activation of the myeloperoxidase system present in both macrophages and PMNL and is controlled by various cytokines [1, 58]. The damaging effect of the infection is shown by the fact that leukocytes in an activated state are able to produce a 100-fold increase in the concentration of ROS when compared to leukocytes that are not activated [59]. This rapid and high increase of OS is an example of how damaging the condition of leukocytospermia can be.

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