Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (668 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Infiltration of inflammatory cells into the parenchyma of prostate. The subtypes are classified by their varied laboratory analysis, clinical presentation and response to treatment.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Prostatitides; Acute Bacterial Prostatitis; Acute Bacterial Prostatitides; Bacterial Prostatitides, Acute; Bacterial Prostatitis, Acute; Chronic Bacterial Prostatitis; Bacterial Prostatitides, Chronic; Bacterial Prostatitis, Chronic.
Where it fits in the MeSH classification
- Broader topics
- Prostatic Diseases
Related concepts
Research landscape
PubMed indexes 6,369 records tagged with the MeSH heading “Prostatitis” (counts retrieved 2026-11-04). 879 of them (13.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 2,590 records.
Reviews account for 921 records (14.5%) and meta-analyses for 71. Randomized controlled trials number 319 (5.0%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,590 |
| 2000-2009 | 1,452 |
| 2010-2019 | 1,448 |
| 2020 onward | 879 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 921 | 14.5% |
| Meta-analyses | 71 | 1.1% |
| Randomized controlled trials | 319 | 5.0% |
Method: PubMed query "Prostatitis"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in kidney, urology and women's health
Kidney, urinary and reproductive health research uses lab markers (such as creatinine), imaging, symptom scores and registry data on pregnancy and birth. Findings about pregnancy are especially sensitive to who was studied and when in pregnancy exposure occurred. Nothing on this page is advice about treatment, fertility or pregnancy; speak to a qualified clinician. Check the population, the outcome measured and whether the study accounted for other health differences between groups.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Multi-faceted immunomodulatory and tissue-tropic clinical bacterial isolate potentiates prostate cancer immunotherapy | 2018 | Research article Design not recorded in structured metadata | 87 | cc by PMID 29686284 · DOI · PMC5913311 |
| TNF is a potential therapeutic target to suppress prostatic inflammation and hyperplasia in autoimmune disease | 2022 | Research article Design not recorded in structured metadata | 73 | cc by PMID 35440548 · DOI · PMC9018703 |
| Current Knowledge of the Potential Links between Inflammation and Prostate Cancer | 2019 | Review article Design not recorded in structured metadata | 70 | cc by PMID 31390729 · DOI · PMC6696519 |
| Epithelial redox stress programs macrophage immunometabolism through a ZNF24-MIF-NF-κB pathway in chronic nonbacterial prostatitis | 2026 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41576699 · DOI · PMC12859805 |
Multi-faceted immunomodulatory and tissue-tropic clinical bacterial isolate potentiates prostate cancer immunotherapy [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Immune checkpoint inhibitors have not been effective for immunologically "cold" tumors, such as prostate cancer, which contain scarce tumor infiltrating lymphocytes.
- Closing excerpt
- CP1 is an immunotherapeutic tool demonstrating how a tissue-specific microbe can increase tumor immunogenicity and sensitize an otherwise resistant cancer type to immunotherapy.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Immune checkpoint inhibitors have not been effective for immunologically "cold" tumors, such as prostate cancer, which contain scarce tumor infiltrating lymphocytes. We hypothesized that select tissue-specific and immunostimulatory bacteria can potentiate these immunotherapies. Here we show that a patient-derived prostate-specific microbe, CP1, in combination with anti-PD-1 immunotherapy, increases survival and decreases tumor burden in orthotopic MYC- and PTEN-mutant prostate cancer models. CP1 administered intra-urethrally specifically homes to and colonizes tumors without causing any systemic toxicities. CP1 increases immunogenic cell death of cancer cells, T cell cytotoxicity, and tumor infiltration by activated CD8 T cells, Th17 T cells, mature dendritic cells, M1 macrophages, and NK cells. CP1 also decreases intra-tumoral regulatory T cells and VEGF. Mechanistically, blocking CP1-recruited T cells from infiltrating the tumor inhibits its therapeutic efficacy. CP1 is an immunotherapeutic tool demonstrating how a tissue-specific microbe can increase tumor immunogenicity and sensitize an otherwise resistant cancer type to immunotherapy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29686284 · DOI · PMC5913311
TNF is a potential therapeutic target to suppress prostatic inflammation and hyperplasia in autoimmune disease [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Autoimmune (AI) diseases can affect many organs; however, the prostate has not been considered to be a primary target of these systemic inflammatory processes.
- Closing excerpt
- Together, these studies show that patients with AI diseases have a heightened susceptibility to BPH and that reducing inflammation with a therapeutic agent can suppress BPH.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (155 words)
Autoimmune (AI) diseases can affect many organs; however, the prostate has not been considered to be a primary target of these systemic inflammatory processes. Here, we utilize medical record data, patient samples, and in vivo models to evaluate the impact of inflammation, as seen in AI diseases, on prostate tissue. Human and mouse tissues are used to examine whether systemic targeting of inflammation limits prostatic inflammation and hyperplasia. Evaluation of 112,152 medical records indicates that benign prostatic hyperplasia (BPH) prevalence is significantly higher among patients with AI diseases. Furthermore, treating these patients with tumor necrosis factor (TNF)-antagonists significantly decreases BPH incidence. Single-cell RNA-seq and in vitro assays suggest that macrophage-derived TNF stimulates BPH-derived fibroblast proliferation. TNF blockade significantly reduces epithelial hyperplasia, NFκB activation, and macrophage-mediated inflammation within prostate tissues. Together, these studies show that patients with AI diseases have a heightened susceptibility to BPH and that reducing inflammation with a therapeutic agent can suppress BPH.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35440548 · DOI · PMC9018703
Current Knowledge of the Potential Links between Inflammation and Prostate Cancer [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Inflammation is inherent in prostatic diseases and it is now accepted that it may facilitate cellular proliferation in both benign and malignant conditions.
- Closing excerpt
- In this perspective, evaluation of the inflammatory component in prostate specimens could be included in routine pathology reports.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (115 words)
Inflammation is inherent in prostatic diseases and it is now accepted that it may facilitate cellular proliferation in both benign and malignant conditions. The strong relationship between prostatic inflammation and pathogenesis of benign prostatic hyperplasia (BPH) is supported by epidemiologic, histopathologic and molecular evidence. Contrariwise, the role of inflammation in prostate carcinogenesis is still controversial, although current data indicate that the inflammatory microenvironment can regulate prostate cancer (PCa) growth and progression. Knowledge of the complex molecular landscape associated with chronic inflammation in the context of PCa may lead to the introduction and optimization of novel targeted therapies. In this perspective, evaluation of the inflammatory component in prostate specimens could be included in routine pathology reports.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31390729 · DOI · PMC6696519
Epithelial redox stress programs macrophage immunometabolism through a ZNF24-MIF-NF-κB pathway in chronic nonbacterial prostatitis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Chronic nonbacterial prostatitis (CNP) is a prevalent and refractory urogenital disorder whose immunopathogenic mechanisms remain incompletely understood.
- Closing excerpt
- Moreover, multiple redox-sensitive nodes within this pathway represent promising therapeutic targets for precision immunomodulation in CNP.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (248 words)
Chronic nonbacterial prostatitis (CNP) is a prevalent and refractory urogenital disorder whose immunopathogenic mechanisms remain incompletely understood. Given that redox imbalance is increasingly recognized as a critical driver of chronic inflammation, this study systematically investigated the role of epithelial redox stress in immune regulation during CNP and its underlying molecular mechanisms. By integrating plasma cytokine profiling, bulk and single-cell transcriptomic analyses, and experimental autoimmune prostatitis (EAP) models, we identified epithelial-derived macrophage migration inhibitory factor (MIF) as a central mediator driving chronic prostatic inflammation. Mechanistically, inflammatory injury induced excessive accumulation of reactive oxygen species (ROS) in epithelial cells, which in turn activated the redox-responsive transcription factor ZNF24 to bind the MIF promoter and promote its transcription. Epithelial cell-derived MIF acted in a paracrine manner on CD74-expressing macrophages. Engagement of CD74 by MIF stabilized PKM2 expression, enhanced macrophage glycolytic reprogramming, promoted PKM2 nuclear translocation, and activated NF-κB-dependent transcriptional programs, thereby driving M1 macrophage polarization and proinflammatory cytokine production. Pharmacological interventions targeting distinct key nodes of this signaling pathway-including inhibition of MIF (ISO-1), blockade of CD74 (neutralizing antibodies), stabilization of PKM2 tetramers (DASA-58), and suppression of NF-κB (JSH-23)-significantly attenuated prostatic inflammation, restored mitochondrial homeostasis, and alleviated pelvic pain in vitro or in vivo. Collectively, these findings define an epithelial ROS-ZNF24-MIF-macrophage CD74-PKM2-NF-κB signaling axis, through which coordinated enhancement of glycolytic reprogramming and inflammatory signaling promotes M1 macrophage polarization and drives the initiation and progression of CNP. Moreover, multiple redox-sensitive nodes within this pathway represent promising therapeutic targets for precision immunomodulation in CNP.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41576699 · DOI · PMC12859805
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Epidemiology of prostatitis [5]
- Research article Role of oxidative stress, infection and inflammation in male infertility [6]
- Research article Management of chronic prostatitis/chronic pelvic pain syndrome: a systematic review and network meta-analysis [7]
- Research article The microbiome in prostate inflammation and prostate cancer [8]
- Research article Treatment of bacterial prostatitis [9]
- Research article Chronic prostatitis/chronic pelvic pain syndrome: a review of evaluation and therapy [10]
References
- Anker JF, Naseem AF, Mok H, Schaeffer AJ, Abdulkadir SA, Thumbikat P. Multi-faceted immunomodulatory and tissue-tropic clinical bacterial isolate potentiates prostate cancer immunotherapy. . 2018. PMID 29686284 · DOI · PMC5913311
- Vickman RE, Aaron-Brooks L, Zhang R, Lanman NA, Lapin B, Gil V, et al.. TNF is a potential therapeutic target to suppress prostatic inflammation and hyperplasia in autoimmune disease. . 2022. PMID 35440548 · DOI · PMC9018703
- Cai T, Santi R, Tamanini I, Galli IC, Perletti G, Bjerklund Johansen TE, et al.. Current Knowledge of the Potential Links between Inflammation and Prostate Cancer. . 2019. PMID 31390729 · DOI · PMC6696519
- Zhang F, Zhang A, Meng T, Liu X, Yang C, Liang C, et al.. Epithelial redox stress programs macrophage immunometabolism through a ZNF24-MIF-NF-κB pathway in chronic nonbacterial prostatitis. . 2026. PMID 41576699 · DOI · PMC12859805
- Krieger JN, Lee SW, Jeon J, Cheah PY, Liong ML, Riley DE. Epidemiology of prostatitis. Int J Antimicrob Agents. 2008. PMID 18164907 · DOI · PMC2292121
- Agarwal A, Rana M, Qiu E, AlBunni H, Bui AD, Henkel R. Role of oxidative stress, infection and inflammation in male infertility. Andrologia. 2018. PMID 30569652 · DOI
- Anothaisintawee T, Attia J, Nickel JC, Thammakraisorn S, Numthavaj P, McEvoy M, et al.. Management of chronic prostatitis/chronic pelvic pain syndrome: a systematic review and network meta-analysis. JAMA. 2011. PMID 21205969 · DOI
- Porter CM, Shrestha E, Peiffer LB, Sfanos KS. The microbiome in prostate inflammation and prostate cancer. Prostate Cancer Prostatic Dis. 2018. PMID 29795140 · DOI
- Lipsky BA, Byren I, Hoey CT. Treatment of bacterial prostatitis. Clin Infect Dis. 2010. PMID 20459324 · DOI
- Polackwich AS, Shoskes DA. Chronic prostatitis/chronic pelvic pain syndrome: a review of evaluation and therapy. Prostate Cancer Prostatic Dis. 2016. PMID 26951713 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.