Testosterone and estradiol modify the expression of adhesins and biofilm formation in Actinobacillus seminis

Abstract

Actinobacillus seminis is the causal agent of epididymitis and has other effects on the reproductive tracts of small ruminants and bovines. This bacterium causes infection when luteinizing (LH) or follicle-stimulating hormones increase, and hosts reach sexual maturity. LH induces female ovulation and male testosterone production, suggesting that these hormones affect A. seminis pathogenicity. In the present study, we evaluated the effect of testosterone (1-5 ng/mL) or estradiol (5–25 pg/mL) added to culture medium on the in vitro growth, biofilm production, and adhesin expression of A. seminis. Estradiol does not promote the growth of this bacterium, whereas testosterone increased A. seminis planktonic growth twofold. Both hormones induced the expression of the elongation factor thermo unstable (EF-Tu) and phosphoglycerate mutase (PGM), proteins that A. seminis uses as adhesins. Estradiol (5 or 10 pg/mL) decreased biofilm formation by 32%, whereas testosterone, even at 5 ng/mL, showed no effect. Both hormones modified the concentrations of carbohydrates and eDNA in biofilms by 50%. Amyloid proteins are characterized by their capacity to bind Congo red (CR) dye. A. seminis binds CR dye, and this binding increases in the presence of 5 to 20 pg/mL estradiol or 4 ng/mL testosterone. The A. seminis EF-Tu protein was identified as amyloid-like protein (ALP). The effect of sexual hormones on the growth and expression of virulence factors of A. seminis seems to be relevant for its colonization and permanence in the host.

Testosterone increases the virulence traits of uropathogenic Escherichia coli

“…However, we have not found any prior references to testosterone inducing increased E. coli growth. Yet, testosterone was shown to increase Actinobacillus seminist growth ( Ramírez-Paz-Y-Puente et al, 2023 ). As bacterial growth is strongly associated with UTIs ( Anderson et al, 2004 ), these findings may be a contributing factor explaining why women are more prone to UTI after menopause.…”