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Insights from Immunomics and Metabolomics on the Associations Between Prostatic Diseases and Coronavirus Disease 2019

Overview
Journal Prostate Int
Date 2025 Jan 16
PMID 39816935
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Abstract

Background: The causal associations and potential mechanisms between prostatic diseases, the predominant male urological disorders, and the course of COVID-19 remain unclear.

Methods: A two-sample Mendelian randomization (MR) analysis was performed to evaluate causal associations between prostate cancer, benign prostatic hyperplasia, and prostatitis and different COVID-19 outcomes (SARS-CoV-2 infection, hospitalized COVID-19, and severe COVID-19). Reverse MR, linkage disequilibrium score regression, and Bayesian colocalization analyses were subsequently performed to strengthen the identified causal relationships. Furthermore, immunome- and metabolome-wide MR analysis was conducted to prioritize COVID-19-associated immune characteristics and metabolites. Two-step MR analysis was performed to evaluate the mediating effects of the immunome and metabolome on the associations between prostatic diseases and COVID-19.

Results: Genetically predicted prostatic diseases were not causally associated with severe COVID-19, while prostatitis was suggested to be an independent risk factor for SARS-CoV-2 infection (odds ratio (OR) = 1.11, 95% confidence interval (CI) 1.01 to 1.23;  = 0.03). Multiple sensitivity tests verified the reliability of the established causal relationships. Dozens of blood immune and metabolic features were identified to reveal the immune and metabolic profiles of different COVID-19 courses. Moreover, PDL-1 on monocyte was found to mediate the interaction between prostatitis and SARS-CoV-2 infection, with a mediation proportion of 9.2%.

Conclusion: Our study identified the causal relationships of prostatic diseases with COVID-19 and suggested pathways explaining these associations through alterations in the blood immunome and metabolome.

References
1.
Rutkowska E, Kwiecien I, Klos K, Rzepecki P, Chcialowski A . Intermediate Monocytes with PD-L1 and CD62L Expression as a Possible Player in Active SARS-CoV-2 Infection. Viruses. 2022; 14(4). PMC: 9031659. DOI: 10.3390/v14040819. View

2.
Borsellino G, Kleinewietfeld M, Di Mitri D, Sternjak A, Diamantini A, Giometto R . Expression of ectonucleotidase CD39 by Foxp3+ Treg cells: hydrolysis of extracellular ATP and immune suppression. Blood. 2007; 110(4):1225-32. DOI: 10.1182/blood-2006-12-064527. View

3.
Stephenson E, Reynolds G, Botting R, Calero-Nieto F, Morgan M, Tuong Z . Single-cell multi-omics analysis of the immune response in COVID-19. Nat Med. 2021; 27(5):904-916. PMC: 8121667. DOI: 10.1038/s41591-021-01329-2. View

4.
Berezhnoy G, Bissinger R, Liu A, Cannet C, Schafer H, Kienzle K . Maintained imbalance of triglycerides, apolipoproteins, energy metabolites and cytokines in long-term COVID-19 syndrome patients. Front Immunol. 2023; 14:1144224. PMC: 10203989. DOI: 10.3389/fimmu.2023.1144224. View

5.
Looi M . Covid-19: WHO adds JN.1 as new variant of interest. BMJ. 2023; 383:2975. DOI: 10.1136/bmj.p2975. View