Microbiota of Urine, Glans and Prostate Biopsies in Patients with Prostate Cancer Reveals a Dysbiosis in the Genitourinary System

Abstract

Prostate cancer (PCa) is the most common malignant neoplasm with the highest worldwide incidence in men aged 50 years and older. Emerging evidence suggests that the microbial dysbiosis may promote chronic inflammation linked to the development of PCa. Therefore, this study aims to compare the microbiota composition and diversity in urine, glans swabs, and prostate biopsies between men with PCa and non-PCa men. Microbial communities profiling was assessed through 16S rRNA sequencing. The results indicated that α-diversity (number and abundance of genera) was lower in prostate and glans, and higher in urine from patients with PCa, compared to non-PCa patients. The different genera of the bacterial community found in urine was significantly different in PCa patients compared to non-PCa patients, but they did not differ in glans and prostate. Moreover, comparing the bacterial communities present in the three different samples, urine and glans show a similar genus composition. Linear discriminant analysis (LDA) effect size (LEfSe) analysis revealed significantly higher levels of the genera Streptococcus, Prevotella, Peptoniphilus, Negativicoccus, Actinomyces, Propionimicrobium, and Facklamia in urine of PCa patients, whereas Methylobacterium/Methylorubrum, Faecalibacterium, and Blautia were more abundant in the non-PCa patients. In glans, the genus Stenotrophomonas was enriched in PCa subjects, while Peptococcus was more abundant in non-PCa subjects. In prostate, Alishewanella, Paracoccus, Klebsiella, and Rothia were the overrepresented genera in the PCa group, while Actinomyces, Parabacteroides, Muribaculaceae sp., and Prevotella were overrepresented in the non-PCa group. These findings provide a strong background for the development of potential biomarkers with clinical interest.

Opportunistic pathogen Porphyromonas gingivalis targets the LC3B-ceramide complex and mediates lethal mitophagy resistance in oral tumors

“… 68 In this study, although we did not measure P. gingivalis -generated phosphoglycerol dihydroceramides or phosphoethanolamine dihydroceramides after infection of OSCC cells, P. gingivalis infection prevented ceramide-dependent mitophagy in both xenograft-derived human OSCC tumors and allograft-derived murine orthotopic OSCC tumors in response to LCL768 in vivo . Further, our 16S rRNA sequencing data showed an increased presence of Gordonia , 69 Stenotrophomonas , 70 , 71 , 72 , 73 and Herbaspirillum 74 , 75 in P. gingivalis- infected tumors that showed resistance to LCL768-induced mitophagy in in vivo orthotopic OSCC tumors. Whether increased levels of these bacteria in the tumor macroenvironment play any independent or synergistic roles in the modulation of lethal mitophagy in response to LCL768 in OSCC tumors is unknown.…”

Causal relationships between gut microbiota, immune cell, and Non-small cell lung cancer: a two-step, two-sample Mendelian randomization study

“…It could utilize organic nutrients through fermentation metabolism and produce H 2 from peptone without utilizing carbohydrates [28]. Studies illustrated that the abundance of Genus-Peptococcus in several cancers was significantly decreased, like prostate cancer and gastric cancer, and was closely related to cancer cachexia [29][30][31]. However, so far, there is no research indicating whether there are differences in the composition and distribution of Genus-Peptococcus in NSCLC.…”

Prostate Tissue Microbiome in Patients with Prostate Cancer: A Systematic Review

“…Only five out of the nine included articles, mention performing a diversity analysis. Out of those five articles, Sarkar et al, Salachan et al, and Gonçalves et al reported that their alpha diversity assessment indicated a lower species richness in samples from the malignant group than those in the benign (control) groups [38,40,41]. However, Feng et al and Cavarretta et al were not able to distinguish between benign and malignant groups with alpha or beta diversity [35,37].…”

“…In contrast, they obtained the benign tissue controls from patients with benign prostatic hyperplasia (BPH) who underwent transurethral resection of the prostate [34,39]. Two studies used transrectal ultrasound-guided prostate biopsies to obtain tissue samples for both their benign control and experimental groups [38,41]. Only one study used mRNA-seq data downloaded from EBI ENA [36].…”

“…At the genus level, Rickettsia [34], Mycobacterium [34], Bordetella [34], Mycoplasma [34,39], Sphingomonas [34], Bartonella [34], Helicobacter [34], Bacillus [34], Porphyromonas [34], Salmonella [34], Aeromonas [34], Brevundimonas [34], Shigella [34], Staphylococcus [35], Streptococcus [35], Cutibacterium [36,38,41], Lawsonella [38], Shewanella [40], Prevotella [41], Cupriavidus [41], and Methylobacterium [41] were found to be significantly increased in the prostate cancer cohort in several of the studies that were analyzed. However, in two studies, Prevotella and Staphylococcus were reported to be significantly more abundant in the benign groups versus the prostate cancer groups [38,40]. The other genera found to be particularly increased in the benign cohorts were Cellvibrio [41], Kocuria [41], Vibrio [40], Bacteroides [40], Chlamydia [34], Pseudomonas [34], Burkholderia [34], Campylobacter [34].…”