Summary. Many studies have examined the impact of genital tract infections on male fertility; however, the effect of bacteriospermia on sperm quality is still controversial. Bacterial infections are more frequently found in semen samples from asymptomatic infertile patients than in those from fertile men. Bacteriospermia is also a common problem of male partners from couples undergoing IVF. Therefore, the effects of microorganisms on human sperm acrosome reaction of oocytes have been studied in vitro and in vivo. Incubation of spermatozoa with Escherichia coli or Mycoplasma hominis in vitro resulted in reduced sperm motility and inducibility of acrosome reaction (ΔAR) after exposure to calcium ionophore A23187. To show possible effects of E. coli and mycoplasma species on sperm functions in vivo, data from 488 patients were evaluated, in whose ejaculates microbiological examinations and determinations of acrosome reaction after exposure to low temperature had been performed. U. urealyticum and E. coli were found in semen samples from 52 and 31 men, respectively. M. hominis was only present in a minor number of samples and was not included in this study. Semen concentrations of E. coli and U. urealyticum ranged between 500–100000 cfu x ml−1 and 100–80000 cfu x ml−1. No correlation was found between ΔAR and concentration of bacteria (Spearman rank correlation coefficient, E. coli: r‐0.081, P = 0.6644; U. urealyticum: r = ‐0.081, P = 0.5698). In 69% of cases with U. urealyticum infection and reduced inducibility of acrosome reaction, this sperm function was normal after antibiotic therapy. However, improvement of acrosomal function may only be due to intra‐individual variations of acrosome reaction. While E. coli and mycoplasma species affect sperm functions in vitro, the present data and a review of the literature fail to demonstrate similar effects in vivo.

Summary The presence of components of the renin angiotensin system (RAS) and specific receptors of angiotensin II in the female and male reproductive tract supports the hypothesis that reproductive functions may be controlled by RAS. Therefore, the present study investigated the influence of ACE and angiotensins on sperm functions and the sperm–egg interaction. The experiments did not indicate direct effects of ACE on the capacitation process or acrosome reaction. Release of ACE from human spermatozoa during capacitation was not related to their ability to undergo acrosome reaction after stimulation with ionophore. Therefore, ACE release does not seem to be a useful clinical marker for human sperm capacitation. However, decreased binding of human spermatozoa to the oolemma of zona‐free hamster oocytes after inhibition of ACE by captopril indicates that kininase II is involved in sperm–egg interactions. In contrast to other studies, incubation with captopril had no influence on sperm binding to the zona pellucida. Because effects of ACE on sperm–egg interactions but not on capacitation or acrosome reaction were observed, several experiments were performed to study the influence of substrates and products on the acrosome reaction. Angiotensin II induced the acrosome reaction dose‐dependently, whereas angiotensin I had no effect on the acrosome reaction. The effect of angiotensin II on acrosome reaction seems to be calcium‐dependent and mediated by protein kinases. Since a specific type 2 angiotensin II receptor inhibits the acrosome reaction induced by angiotensin II, this subtype of receptors may be present at the surface of sperm heads. Another clue for the presence of type 2 receptors on human spermatozoa is the finding that pertussis toxin did not inhibit the angiotensin II induced acrosome reaction. In contrast to type 1 angiotensin II receptors, type 2 receptors are known to be G‐protein independent.

Obesity is a risk factor for erectile dysfunction and atherosclerosis. Lipocalin‐2 is an adipocytokine with proinflammatory properties involved in several disorders with metabolic alterations. Our aim was to study the relation of serum lipocalin‐2 and carotid artery intima–media thickness (CIMT) to obesity in erectile dysfunction. Serum lipocalin‐2 and CIMT were measured in 25 obese and 25 nonobese eugonadal patients over forty with venogenic erectile dysfunction and 25 healthy controls. Their relation to different patient‐ and disease‐related parameters was studied. Results revealed lipocalin‐2 to be significantly higher in obese compared with nonobese patients and with controls, and in nonobese patients compared with controls. CIMT was lower in controls compared with both obese and nonobese patients. In obese and nonobese patients, lipocalin‐2 was positively correlated with disease duration, body mass index, waist circumference and end‐diastolic velocity. Lipocalin‐2 was negatively correlated with the short form of the international index of erectile function scores in both groups. In conclusion, the elevated lipocalin‐2 in obese and to a lesser extent in nonobese patients and its association with disease severity points to its potential value as a diagnostic marker and a possible therapeutic target that could ameliorate the metabolic derangement associated with erectile dysfunction.

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The transcriptomic regulation induced by isotretinoin (13-cis retinoic acid) is still a matter of debate as short-term exposures of immortalized sebocytes with isotretinoin produced conflicting results. Based on translational evidence, it has been hypothesized that oral isotretinoin treatment upregulates the expression of the transcription factor p53. Twenty-five patients suffering from acne vulgaris were treated with isotretinoin (0.6 mg/kg body weight) for 6 weeks. Biopsies from back skin were taken before and after isotretinoin treatment for the determination of p53 expression by immunohistochemical staining, quantification of p53 protein concentration by enzyme-linked immunosorbent assay and TP53 gene expression by quantitative reverse transcription real time PCR. Fifteen socio-demographically cross-matched healthy volunteers served as controls. Isotretinoin treatment significantly increased the nuclear expression of p53 in sebaceous glands of treated patients compared to pre-treatment levels and p53 levels of untreated controls. Furthermore, the p53 protein and gene expression significantly increased in the skin after treatment. The magnitude of p53 expression showed an inverse correlation to acne severity score and body mass index. Under clinical conditions, isotretinoin induced the expression of p53, which controls multiple transcription factors involved in the pathogenesis of acne vulgaris including FoxO1, androgen receptor and critical genes involved in the induction of autophagy and apoptosis. Increased p53-FoxO1 signalling enhanced by systemic isotretinoin treatment explains the underlying transcriptomic changes causing sebum suppression but also the adverse effects associated with systemic isotretinoin therapy.