Differential Changes of Corticotropin Releasing Hormone (CRH) Concentrations in Plasma and Synovial Fluids of Patients with Rheumatoid Arthritis (RA).

Nishioka, Tatsuya; Kurokawa, Hisayo; Takao, Toshihiro; Kumon, Yoshitaka; Nishiya, Koji; Hashimoto, Kozo

doi:10.1507/endocrj.43.241

Cited by 24 publications

(10 citation statements)

References 23 publications

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“…Likewise, CRF was found to cause the release of cytokines such as IL-1, IL-2, and IL-6 from immune cells in vitro (Leu & Singh, 1992;Paez Pereda et al, 1995;Singh & Leu, 1990), to induce synthesis of acute phase proteins from liver hepatocytes (Hagan, Poole, & Bristow, 1993), and to stimulate the release of IL-1 from hypothalamic explants (Tringali et al, 1997). These ®ndings have culminated in the suggestion that CRF overproduction is involved in in¯ammatory disease states such as experimental uveitis (Mastorakos et al, 1995) and rheumatoid arthritis (Nishioka et al, 1996;Webster, Torpy, Elenkov, & Chrousos, 1998), which may be precipitated or exacerbated by exposure to stressors (e.g., Zautra et al, 1997). Because peripheral IL-1 can activate vagal afferents, which in turn can result in increased IL-1 in the brain (Hosoi, Okuma, & Nomura, 2000;Laye et al, 1995), there exists at least one empirically testable pathway by which peripheral CRF might, by means of stimulating peripheral cytokine activity, induce central cytokine activity such as is known to underlie sickness behaviors.…”

Section: Separation and Sickness Behaviormentioning

confidence: 97%

Stress‐induced sickness behaviors: An alternative hypothesis for responses during maternal separation

Hennessy

Deak

Schiml-Webb

2001

Developmental Psychobiology

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During maternal separation, some primate and nonprimate species show a biphasic (active/passive) response. The second stage is characterized by reduced activity, a hunched body posture, and other behaviors. Traditionally, the second stage has been referred to as "despair" and is considered an animal model for human depression. Recent research in psychoneuroimmunology suggests an alternative hypothesis--that behaviors occurring during the second passive phase represent stress-induced "sickness behaviors." This perspective more readily accounts for findings in widely divergent species, does not require assumptions regarding the ability to express complex emotional states, is empirically testable, and aligns the separation model with recent hypotheses regarding the nature and ontogeny of depressive illness.

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Section: Separation and Sickness Behaviormentioning

confidence: 97%

Stress‐induced sickness behaviors: An alternative hypothesis for responses during maternal separation

Hennessy

Deak

Schiml-Webb

2001

Developmental Psychobiology

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“…In addition, during the process of inflammatory stress, various cytokines stimulate CRF secretion at local inflammatory sites, such as in the arthritic joint, but its action appears to be proinflammatory. Nishioka et al [37] reported that concentrations of CRF and interleukin-6 in synovial fluid were higher in RA patients than in OA patients, but that plasma corticotropin and CRF levels were significantly lower in RA patients than in OA patients. This may suggest that the secretion of CRF in synovial fluid is regulated differently from plasma CRF secretion, since CRF levels in the synovial fluid and plasma of RA patients showed opposite trends.…”

Section: Rt-pcr Of Urocortin and Crf-rs In Synovial Tissuementioning

confidence: 99%

Urocortin in the synovial tissue of patients with rheumatoid arthritis

et al. 2001

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Urocortin is a newly identified member of the corticotropin-releasing factor (CRF) neuropeptide family, and is known to be involved in the modulation of the inflammatory process. We examined the expression of urocortin, CRF and their receptors (CRF receptor; CRF-R) in the synovial tissue of patients with rheumatoid arthritis (RA) in order to study the possible biological roles of urocortin. Synovial tissues/fluids were obtained from 38 patients with RA, nine patients with osteoarthritis and four with trauma. We studied the concentration of urocortin in the synovial fluid using RIA, and the expression of urocortin in synovial tissue using immunohistochemistry, mRNA in situ hybridization and reverse transcriptase-PCR (RT-PCR). In addition, we examined the immunolocalization of CRF and the expression of CRF-R1, -R2-alpha and -R2-beta mRNAs utilizing RT-PCR in these synovial tissues. Urocortin concentrations in synovial fluid were higher in RA patients (79.8+/-154 pg/ml) than in control patients (12.3+/-4.8 pg/ml; P< or =0.05). Urocortin immunoreactivity and mRNA signals were both detected in synovial cells, lymphocytes, fibroblasts and macrophages. The number of urocortin-positive cells in the synovium was significantly higher in RA (73.1+/-32.1 cells per high-power field) than in control (18.4+/-10.4 cells per high-power field) patients. In addition, both urocortin immunoreactivity and mRNA signals in the synovium reached maximum levels in the active stage of RA inflammation. Moreover, the number of immunoreactive urocortin-positive cells was significantly correlated with the urocortin concentration in synovial fluid (r=0.705; P<0.001) and with histologically defined local inflammatory activity (r=0.641; P<0.001). The distribution and number of immunoreactive CRF-positive cells in synovial tissue were similar to those of urocortin-positive cells (r=0.701; P<0.001). Urocortin, CRF-R1 and CRF-R2-alpha mRNAs detected by RT-PCR were expressed in in the synovium of 10/10, 10/10 and 2/10 RA patients respectively, but CRF-R2-beta was not expressed. Urocortin was actively synthesized in the synovium of RA patients. The present study suggests that urocortin may play an important role as an autocrine and/or paracrine regulator of synovial inflammation in RA.

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“…This would culminate in inflammation and lowered pain threshold. 7 The CRH levels detected in the synovial fluid from RA patients, although lower than in osteoarthritis, 20 has the propensity to increase IL-6, 18 from macrophages and increase its activity after combining with CRHbinding protein, 21 and needs further research for its role in RA inflammation. …”

Section: Discussionmentioning

confidence: 99%

Genetic analysis of CRHRA1 and CRHRA2 microsatellites and their association with rheumatoid arthritis in South Asian and Caucasian populations of the East Midlands, UK.

Ghelani

Steer²,

Fisher

et al. 2012

Rheumatol Rep

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Differential Changes of Corticotropin Releasing Hormone (CRH) Concentrations in Plasma and Synovial Fluids of Patients with Rheumatoid Arthritis (RA).

Cited by 24 publications

References 23 publications

Stress‐induced sickness behaviors: An alternative hypothesis for responses during maternal separation

Stress‐induced sickness behaviors: An alternative hypothesis for responses during maternal separation

Urocortin in the synovial tissue of patients with rheumatoid arthritis

Genetic analysis of CRHRA1 and CRHRA2 microsatellites and their association with rheumatoid arthritis in South Asian and Caucasian populations of the East Midlands, UK.

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