How Finasteride could directly work against Microbes

Seeing what could be possible here. Genes that almost mimic humans, including 5ar.
One example,

In vitro analysis of finasteride activity against Candida albicans urinary biofilm formation and filamentation.

https://www.ncbi.nlm.nih.gov/pubmed/25049253
Candida albicans is the 3rd most common cause of catheter-associated urinary tract infections, with a strong propensity to form drug-resistant catheter-related biofilms. Due to the limited efficacy of available antifungals against biofilms, drug repurposing has been investigated in order to identify novel agents with activities against fungal biofilms. Finasteride is a 5-α-reductase inhibitor commonly used for the treatment of benign prostatic hyperplasia, with activity against human type II and III isoenzymes. We analyzed the Candida Genome Database and identified a C. albicans homolog of type III 5-α-reductase, Dfg10p, which shares 27% sequence identity and 41% similarity to the human type III 5-α-reductase. Thus, we investigated finasteride for activity against C. albicans urinary biofilms, alone and in combination with amphotericin B or fluconazole. Finasteride alone was highly effective in the prevention of C. albicans biofilm formation at doses of ≥16 mg/liter and the treatment of preformed biofilms at doses of ≥128 mg/liter. In biofilm checkerboard analyses, finasteride exhibited synergistic activity in the prevention of biofilm formation in a combination of 4 mg/liter finasteride with 2 mg/liter fluconazole. Finasteride inhibited filamentation, thus suggesting a potential mechanism of action. These results indicate that finasteride alone is highly active in the prevention of C. albicans urinary biofilms in vitro and has synergistic activity in combination with fluconazole. Further investigation of the clinical utility of finasteride in the prevention of urinary candidiasis is warranted.

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Just to add to this bacteria can synthesize dht at a localized tissue level.

5 alpha reductase activity in human gingiva and gingival fibroblasts in response to bacterial culture supernatants, using [14C]4-androstenedione as substrate.

Abstract

5 alpha-Reduction of androgen substrates is increased in inflamed gingiva. It was therefore relevant to study the effect of bacterial culture supernatants derived from Prevotella intermedius (P.i), Porphyromonas gingivalis (P.g) and Actinobacillus actinomycetemcomitans (A.a) on the metabolism of [14C]4-androstenedione to 5 alpha-dihydrotestosterone (DHT) in gingival tissue and cultured fibroblasts. Chronically inflamed human gingival tissue and cultured gingival fibroblasts from the same source were incubated in duplicate with [14C]4-androstenedione and optimal concentrations of P.i, P.g. and A.a culture supernatants in Eagle’s minimal essential medium in a CO2 incubator for 24 h at 37 degrees C. The metabolites were then extracted, separated and quantified using a radioisotope scanner. There were 87, 50 and 6% increases in DHT synthesis by human gingival tissue in response to the culture supernatants of P.i, P.g and A.a, respectively, over control incubations (n = 3; p < 0.01: Wilcoxon signed-ranked statistic for paired observations). With the cells in culture, all four fibroblast cell lines produced DHT and testosterone from [14C]4-androstenedione in varying amounts. The production of DHT was enhanced in the presence of each the bacterial culture supernatants to varying degrees (P.i 40%, P.g 35% and A.a 40%; p < 0.01). Combinations of the bacterial extracts: (P.i + P.g), (P.i + A.a), (P.g + A.a) and (P.i + P.g + A.a) showed intermediate or suppressor effects on DHT formed compared with individual incubations. Culture supernatants of these pathogens can influence DHT synthesis in fibroblasts, and effect that is modulated by baseline androgen metabolism and the proportion of virulent pathogens present. This may have some bearing on host susceptibility on host and the progression of the periodontal lesion.

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