Assessing chronic pelvic pain syndrome patients: Blood plasma factors and cortisol saliva

Lundh, Dan; Hedelin, Hans; Jönsson, Karin; Gifford, Mervyn; Larsson, D. G. Joakim

doi:10.3109/21681805.2013.769460

Cited by 22 publications

(19 citation statements)

References 36 publications

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“…The pro‐inflammatory cytokine MIF can activate macrophages, inhibit their migration, enhance their phagocytosis, and kill tumor activity, and also play a role in immune‐mediated diseases. Blood plasma levels of MIF and TNF‐α were significantly increased in the CP/CPPS patients . The findings show an immune response extending to the circulatory system, in which MIF makes a significant contribution to CP/CPPS.…”

Section: Cp/cpps Immune Microenvironmentmentioning

confidence: 76%

“…Evidence begins to appear, and this connection also exists in neuropathic pain, such as lumbago . The levels of TNF‐α, IL‐1β, IL‐6, and macrophage migration inhibitory factor (MIF) were pathologically altered in long‐term pain subjects . The pro‐inflammatory cytokine MIF can activate macrophages, inhibit their migration, enhance their phagocytosis, and kill tumor activity, and also play a role in immune‐mediated diseases.…”

Section: Cp/cpps Immune Microenvironmentmentioning

confidence: 99%

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Chronic prostatitis/chronic pelvic pain syndrome and prostate cancer: study of immune cells and cytokines

Liu

Mikrani

Xie

et al. 2019

Fundamemntal Clinical Pharma

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Prostate cancer and prostatitis are both significant health concerns. A large number of studies have established that the occurrence of the two is closely related. However, the most common prostatitis, type III chronic prostatitis/chronic pelvic pain syndromes (CP/CPPS), is reported to not correlate with the occurrence of prostate cancer. Although the etiology of CP/CPPS is unknown, it may be related to the autoimmune mechanism favored by most studies. Manipulating the immune system and targeting tumor microenvironment are promising new methods for the treatment of prostate cancer. Therefore, this review focuses on the immune cells and cytokines of CP/CPPS and prostate cancer from the perspective of biological immunology and immune microenvironment. We discuss T‐regulatory (Treg) and T helper 17 (Th17) cells dysfunction, the abnormal regulation of T helper 1(Th1) and T helper 2 (Th2) cells, macrophages, and their related cytokines as key activators in CP/CPPS. In addition, we discuss the roles of Treg and Th17 cells, Th1 and Th2 cells, and related cytokines in modulating prostate cancer progression. This review highlights the concept that immune cells and cytokines provide a research strategy for the etiology of CP/CPPS and offer potentially promising targets for the treatment of prostate cancer.

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Section: Cp/cpps Immune Microenvironmentmentioning

confidence: 76%

Section: Cp/cpps Immune Microenvironmentmentioning

confidence: 99%

Chronic prostatitis/chronic pelvic pain syndrome and prostate cancer: study of immune cells and cytokines

Liu

Mikrani

Xie

et al. 2019

Fundamemntal Clinical Pharma

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“…The underlying mechanisms associated with prostate inflammation and anti-inflammation activity remain unclear. Several studies have shown that the proinflammatory factors TNF-α and IL-1β were increased in prostatic fluid, seminal plasma, or serum of CP/CPPS patients ( 35 – 37 ). Here, we detected significantly higher serum IL-1β and TNF-α levels in EAP rats compared with normal rats.…”

Section: Discussionmentioning

confidence: 99%

Influence of Experimental Autoimmune Prostatitis on Sexual Function and the Anti-inflammatory Efficacy of Celecoxib in a Rat Model

Zhang

Zhou

et al. 2020

Front. Immunol.

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Experimental autoimmune prostatitis (EAP) is a well-established model induced by an autoimmune response to prostate antigen. The symptomatic, pathological, and immunological characteristics of EAP animals are highly consistent with human chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), which makes EAP an ideal model for this disease. Here, we investigate the influence of EAP on male rat sexual function and the efficacy of anti-inflammatory therapy with celecoxib. EAP rat models were established using male Wistar rats. Rats were randomly assigned to a normal control group, an EAP model group, or an EAP model with celecoxib treatment group (celecoxib group). Behavioral changes, sexual behavioral changes, and erectile function were estimated using an open-field test, a sucrose consumption test, mating experiments, and by intracavernous pressure/mean arterial pressure ratio (ICP/MAP). Histological changes in the prostate were observed by HE staining, and the serum inflammatory factors IL-1β and TNF-α levels were measured by enzyme-linked immunosorbent assay. In addition, serotonin (5-hydroxytryptamine, 5-HT), 5-HT 1A receptor, 5-HT 2C receptor, and serotonin transporter (SERT) expression levels in the hippocampus and spinal cord (T13-L1, L5-S2) were examined by immunohistochemistry and western blot analysis. Results showed that EAP rats exhibited characteristics of depression, decreased sexual drive, premature ejaculation, and increased threshold of penile erection. Moreover, all these changes were effectively alleviated by celecoxib. Significant increases in prostatic interstitial infiltration by inflammatory cells and in serum IL-1β and TNF-α levels were observed in EAP rats, and these were partially reduced by celecoxib. Additionally, the expression pattern of serotonin system regulators in the hippocampus and spinal cord were altered in EAP model rats, including a decrease in 5-HT levels and an increase in 5-HT 1A receptor levels. In conclusion, autoimmune prostatitis impaired rat sexual function, and this was effectively prevented by anti-inflammatory therapy with celecoxib. Moreover, a serotonin system disorder in the central nervous system was likely mediated via inflammation in EAP rats.

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“…Research on the quantification of MIF in saliva has been increasing in various pathologies such as oral squamous cell carcinoma [31], in studies evaluating depressive symptoms [32], and in chronic pelvic pain syndrome [33], among others.…”

Section: Mif In Saliva and Serummentioning

confidence: 99%

Immune Response in Gingival Disease: Role of Macrophage Migration Inhibitory Factor

Ortiz-García¹,

Morales-Velazquez²,

García-Orozco³

et al. 2019

Gingival Disease - A Professional Approach for Treatment and Prevention

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The term periodontal disease encompasses a wide variety of chronic inflammatory conditions of the periodontium, including gingivitis and periodontitis. The gingival disease is an infectious process, which occurs due to the progression of untreated gingivitis. It is characterized by a destructive inflammatory process that affects the supporting tissues of the teeth, which causes the loss of the dental organs. As a result of inflammation, a wide range of cytokines and inflammatory mediators together contribute to tissue degradation and bone resorption. However, some molecules that have not been studied in the inflammatory process of this disease, such as the macrophage migration inhibitory factor (MIF) which is considered an important cytokine of the innate immune system; it is expressed constitutively in immune and nonimmune cells, and it is released immediately against bacterial stimuli, hypoxia, and proliferative signals. MIF has been described in some chronic degenerative, inflammatory, and autoimmune diseases. Previous studies have described that in murine models of periodontitis, MIF promotes the activation and differentiation of osteoclasts that could position this cytokine in the immunopathogenesis of gingival disease in humans.

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Assessing chronic pelvic pain syndrome patients: Blood plasma factors and cortisol saliva

Cited by 22 publications

References 36 publications

Chronic prostatitis/chronic pelvic pain syndrome and prostate cancer: study of immune cells and cytokines

Chronic prostatitis/chronic pelvic pain syndrome and prostate cancer: study of immune cells and cytokines

Influence of Experimental Autoimmune Prostatitis on Sexual Function and the Anti-inflammatory Efficacy of Celecoxib in a Rat Model

Immune Response in Gingival Disease: Role of Macrophage Migration Inhibitory Factor

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