Progesterone attenuates temporomandibular joint inflammation through inhibition of NF-κB pathway in ovariectomized rats

Xue, Xin-Tong; Kou, Xiaoxing; Li, Chenshuang; Bi, Rui-Yun; Meng, Zhen; Wang, Xuedong; Zhou, Yanheng; Gan, Ye‐Hua

doi:10.1038/s41598-017-15285-w

Cited by 30 publications

(19 citation statements)

References 28 publications

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“…Progesterone reduces proinflammatory mediators (i.e., TNF-α, IL-6, IL-1β, and nitric oxide (NO)) and increases IL-10 production by macrophages and monocytes (101). Application of progesterone in a temporomandibular joint inflammation model of ovariectomized rats reduced synovial inflammation and levels of TNF-α and IL-1β (102). In a rat colitis model, progesterone ameliorated disease activity through reduction of TNF-α levels in colon and blood (103).…”

Section: Immunity In Ibdmentioning

confidence: 99%

Modulatory Effects of Pregnancy on Inflammatory Bowel Disease

Giessen

Huang

Woude

et al. 2019

Clin Transl Gastroenterol

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The disease course of autoimmune diseases such as rheumatoid arthritis is altered during pregnancy, and a similar modulatory role of pregnancy on inflammatory bowel disease (IBD) has been proposed. Hormonal, immunological, and microbial changes occurring during normal pregnancy may interact with the pathophysiology of IBD. IBD consists of Crohn's disease and ulcerative colitis, and because of genetic, immunological, and microbial differences between these disease entities, they may react differently during pregnancy and should be described separately. This review will address the pregnancy-induced physiological changes and their potential effect on the disease course of ulcerative colitis and Crohn's disease, with emphasis on the modulation of epithelial barrier function and immune profiles by pregnancy hormones, microbial changes, and microchimerism.

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Section: Immunity In Ibdmentioning

confidence: 99%

Modulatory Effects of Pregnancy on Inflammatory Bowel Disease

Giessen

Huang

Woude

et al. 2019

Clin Transl Gastroenterol

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“…The local application of Complete Freund’s Adjuvant (CFA) to chemically induce arthritis and TMJ pathology is well-established [35, 36]. To determine the contribution of Complete Freund’s Adjuvant (CFA) to TMJ pathology, we examined the effect of exogenous CFA on murine mandibular condyle explants (Fig 5).…”

Section: Resultsmentioning

confidence: 99%

Extracellular matrix turnover and inflammation in chemically-induced TMJ arthritis mouse models

et al. 2019

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The temporomandibular joint (TMJ) is a fibrocartilaginous tissue critical for chewing and speaking. In patients with temporomandibular disorders (TMDs), permanent tissue loss can occur. Recapitulating the complexity of TMDs in animal models is difficult, yet critical for the advent of new therapies. Synovial fluid from diseased human samples revealed elevated levels of tumor necrosis factor alpha (TNF-alpha). Here, we propose to recapitulate these findings in mice by subjecting murine TMJs with TNF-alpha or CFA (Complete Freund’s Adjuvant) in mandibular condyle explant cultures and by local delivery in vivo using TMJ intra-articular injections. Both TNF-alpha and CFA delivery to whole mandibular explants and in vivo increased extracellular matrix deposition and increased cartilage thickness, while TNF-alpha treated explants had increased expression of inflammatory cytokines and degradative enzymes. Moreover, the application of TNF-alpha or CFA in both models reduced cell number. CFA delivery in vivo caused soft tissue inflammation, including pannus formation. Our work provides two methods of chemically induced TMJ inflammatory arthritis through a condyle explant model and intra-articular injection model that replicate findings seen in synovial fluid of human patients, which can be used for further studies delineating the mechanisms underlying TMJ pathology.

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“…The latter is known to play an important role in oligodendrocyte death and demyelination . Oestrogens and progesterone have shown anti‐inflammatory actions by repressing the DNA‐binding activity of nuclear factor‐kappa B (NF‐κB) and transcription of NF‐κB targeted proinflammatory cytokines including TNF‐α . Moreover, progesterone also switches microglial cells from a proinflammatory (M1) to an anti‐inflammatory (M2) phenotype in cuprizone demyelination .…”

Section: Discussionmentioning

confidence: 99%

Changes in neurosteroidogenesis during demyelination and remyelination in cuprizone‐treated mice

Leicaj

Pasquini

Lima

et al. 2018

J Neuroendocrinology

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| INTRODUC TI ONMultiple sclerosis (MS) is a disease of the central nervous system (CNS) leading to the demyelination of white and grey matter, 1 characterised initially in most patients by relapsing-remitting episodes.MS presents loss of oligodendrocytes, axonal injury, neurodegeneration and inflammation. 2,3 A role for steroid hormones has been suggested because the incidence, progression and severity of MS are affected in a sex-dependent manner. 4 Furthermore, the prospective European Pregnancy in Multiple Sclerosis (PRIMS) study has found that the rate of relapse is significantly reduced during the last 3 months of pregnancy, when circulating levels of oestrogens and progesterone are highest, whereas the relapse rate increases during the first 3 months post-partum, coincident with the drop in sex steroid levels. 5 These clinical data suggest that sex steroids might play a beneficial role in this disease. In a preclinical model of MS, testosterone, progesterone and oestradiol, exert anti-inflammatory, promyelinating and neuroprotective effects, reinforcing a possible therapeutic use for these hormones. 6-8 Accordingly, progesterone administration to mice with experimental autoimmune encephalomyelitis (EAE), a common model for MS, has been found to reduce clinical scores and the inflammatory response, and also to prevent demyelination and axonal damage in the spinal cord. [9][10][11][12] In addition to progesterone, treatment with oestrogens reduces the clinical Changes of neurosteroids may be involved in the pathophysiology of multiple sclerosis (MS). The present study investigated whether changes of neurosteroidogenesis also occurred in the grey and white matter regions of the brain in mice subjected to cuprizoneinduced demyelination. Accordingly, we compared the expression of neurosteroidogenic proteins, including steroidogenic acute regulatory protein (StAR), voltage-dependent anion channel (VDAC) and 18 kDa translocator protein (TSPO), as well as neurosteroidogenic enzymes, including the side chain cleavage enzyme (P450scc), 3β-hydroxysteroid dehydrogenase/isomerase and 5α-reductase (5α-R), during the demyelination and remyelination periods. Using immunohistochemistry and a quantitative polymerase chain reaction, we demonstrated a decreased expression of StAR, P450scc and 5α-R with respect to an increase astrocytic and microglial reaction and elevated levels of tumor necrosis factor (TNF)α during the cuprizone demyelination period in the hippocampus, cortex and corpus callosum. These parameters, as well as the glial reaction, were normalised after 2 weeks of spontaneous remyelination in regions containing grey matter. Conversely, persistent elevated levels of TNFα and low levels of StAR and P450scc were observed during remyelination in corpus callosum white matter. We conclude that neurosteroidogenesis/myelination status and glial reactivity are inversely related in the hippocampus and neocortex. Establishing a cause and effect relationship for the measured variables remains a future challenge for understa...

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Progesterone attenuates temporomandibular joint inflammation through inhibition of NF-κB pathway in ovariectomized rats

Cited by 30 publications

References 28 publications

Modulatory Effects of Pregnancy on Inflammatory Bowel Disease

Modulatory Effects of Pregnancy on Inflammatory Bowel Disease

Extracellular matrix turnover and inflammation in chemically-induced TMJ arthritis mouse models

Changes in neurosteroidogenesis during demyelination and remyelination in cuprizone‐treated mice

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