Background: Inflammation is the most prevalent and widespread histological finding in the human prostate, and associates with the development and progression of benign prostatic hyperplasia and prostate cancer. Several factors have been hypothesized to cause inflammation, yet the role each may play in the etiology of prostatic inflammation remains unclear. This study examined the possibility that the common protozoan parasite Toxoplasma gondii induces prostatic inflammation and reactive hyperplasia in a mouse model.
Methods: Male mice were infected systemically with T. gondii parasites and prostatic inflammation was scored based on severity and focality of infiltrating leukocytes and epithelial hyperplasia. We characterized inflammatory cells with flow cytometry and the resulting epithelial proliferation with bromodeoxyuridine (BrdU) incorporation.
Results: We found that T. gondii infects the mouse prostate within the first 14 days of infection and can establish parasite cysts that persist for at least 60 days. T. gondii infection induces a substantial and chronic inflammatory reaction in the mouse prostate characterized by monocytic and lymphocytic inflammatory infiltrate. T. gondii-induced inflammation results in reactive hyperplasia, involving basal and luminal epithelial proliferation, and the exhibition of proliferative inflammatory microglandular hyperplasia in inflamed mouse prostates.
Conclusions: This study identifies the common parasite T. gondii as a new trigger of prostatic inflammation, which we used to develop a novel mouse model of prostatic inflammation. This is the first report that T. gondii chronically encysts and induces chronic inflammation within the prostate of any species. Furthermore, T. gondii-induced prostatic inflammation persists and progresses without genetic manipulation in mice, offering a powerful new mouse model for the study of chronic prostatic inflammation and microglandular hyperplasia.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826344 | PMC |
| http://dx.doi.org/10.1002/pros.23362 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The Anti-Inflammatory Roles of Vitamin D for Improving Human Health.
Curr Issues Mol Biol
November 2024
Department of Family Medicine, Cerrahpasa Medical Faculty, Istanbul University-Cerrahpasa, Istanbul 34098, Turkey.
Vitamin D receptors (VDRs) are present in almost all cells of the immune system, including B cells, T cells, NK (Natural Killer) cells, dendritic cells, and monocytes, as well as the epithelial cells of many organs such as the intestine, pancreas, prostate, lungs, and cardiomyocytes. In addition, some immune cells, including dendritic cells, macrophages, and B and T cells, can synthesize calcitriol by expressing 1α-hydroxylase. Upon binding to VDRs, vitamin D (Vit D) regulates the expression of genes involved in immune responses, including those encoding for cytokines.
View Article and Find Full Text PDFLc-ms-based untargeted metabolomics reveals potential mechanisms of histologic chronic inflammation promoting prostate hyperplasia.
PLoS One
December 2024
Clinical Medical College, North China University of Science and Technology, Tangshan, China.
Background: Chronic prostatitis may be a risk factor for developing proliferative changes in the prostate, although the underlying mechanisms are not entirely comprehended.
Materials And Methods: Fifty individual prostate tissues were examined in this study, consisting of 25 patients diagnosed with prostatic hyperplasia combined with histologic chronic inflammation and 25 patients diagnosed with prostatic hyperplasia alone. We employed UPLC-Q-TOF-MS-based untargeted metabolomics using ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry to identify differential metabolites that can reveal the mechanisms that underlie the promotion of prostate hyperplasia by histologic chronic inflammation.
Objective: Aim: To analyze the mechanisms of regulation of the body's proteolytic systems during inflammation, detection of inflammation markers in blood and prostate secretions in the experimental benign prostatic hyperplasia in rats.
Patients And Methods: Materials and Methods: The study was conducted on 30 male rats on the model of benign prostatic hyperplasia. Rats were randomized as following: the 1st group (n=6) - intact animals; the 2nd group (n=24) - rats with benign prostatic hyperplasia.
Scrotal abscess caused by Candida glabrata in a patient with uncontrolled diabetes mellitus and chronic renal failure.
Rev Inst Med Trop Sao Paulo
December 2024
Balikesir University, Medical Faculty, Infectious Diseases and Clinical Microbiology Department, Balikesir, Turkey.
Candida glabrata is a yeast which incidence has increased in recent years and usually causes urogenital and bloodstream infections. Its resistance to fluconazole hinders C. glabrata infections treatment.
View Article and Find Full Text PDFRadiotherapy and inflammaging: the influence of prostate cancer radiotherapy on systemic inflammation.
World J Urol
December 2024
Department of Therapeutic Radiology and Oncology, Comprehensive Cancer Center, Medical University of Graz, 8036, Graz, Austria.
Purpose: The present study was performed to investigate the association of prostate cancer radiotherapy with inflammaging, a condition characterized by the elevation of inflammatory blood parameters that significantly increases the susceptibility to the occurrence or progression of age-related conditions.
Patients And Methods: A total of 306 patients treated with curative radiotherapy (RT) for prostate cancer were enrolled into the prospective study. Aging-related inflammatory parameters including C-reactive protein (CRP), albumin, fibrinogen, cholesterol, platelet-to-lymphocyte ratio (PLR), and neutrophil-to-lymphocyte ratio (NLR) were analyzed before and at the end of RT, and 3 and 15 months after completion of the RT.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!