NLRP3 Inflammasome Plays an Important Role in the Pathogenesis of Collagen-Induced Arthritis.

نویسندگان

  • Yongfeng Zhang
  • Yi Zheng
  • Hongbin Li
چکیده

OBJECTIVE To investigate the relationship between NLRP3 and the pathogenesis of collagen-induced arthritis. METHODS We used the collagen-induced arthritis (CIA) mouse model. The mice were divided into two groups: the model group (CIA, n = 16) and the control group (Normal, n = 8). The mice were sacrificed seven weeks after immunization. The arthritis score and imaging evaluation (X-rays, Micro-CT, and MRI) were performed. Synovial tissue NLRP3 expression and peripheral blood cytokine levels were analyzed. RESULTS The arthritis score (6.00 ± 2.52), imaging score (4.63 ± 0.92), and synovial tissue NLRP3 expression (4.00 ± 2.03) significantly increased in the CIA mice. The expression of synovial NLRP3 was positively correlated with arthritis clinical and radiographic scores (r = 0.792 and r = 0.669, resp.). CONCLUSIONS The synovial NLRP3 expression increased at the early onset of RA. Synovial NLRP3 expression level was correlated with the clinical arthritis severity and extent of radiological destruction, suggesting that NLRP3 is involved in the pathogenesis of RA.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

P 106: Effects of Dimethyl Sulfoxide on NLRP3 Inflammasome and Alzheimer\'s Disease

Alzheimer's disease (AD), the most ordinary form of dementia and extracellular accumulation of Amyloid-β (Aβ) in senile plaques, is an important and a main event in the pathogenesis of AD. Deposition of Aβ Peptide initiates a spectrum of cellular responses that are interposed by the resident neuroimmune cells of the brain, the microglia. Recently, a novel inflammasome signaling&n...

متن کامل

Hemin Induces the Activation of NLRP3 Inflammasome in N9 Microglial Cells

Background: Hemin is an important sterile component that induces a neuroinflammatory response after intracerebral hemorrhage, in which NLRP3 inflammasome activation has also proved to be involved. Although microglial activation acts as a key contributor in the neuroinflammatory response, the relationship between hemin and NLRP3 in microglia remains poorly understood. Objective: To investigate w...

متن کامل

NLRP3 inflammasome plays a critical role in the pathogenesis of hydroxyapatite-associated arthropathy.

The proinflammatory and catabolic cytokine IL-1β has been implicated in the pathogenesis of osteoarthritis (OA) by mediating synovial inflammation and cartilage degeneration. Although synovial macrophages are suggested to be the source of IL-1β, the mechanism remains unclear. Ectopic deposition of hydroxyapatite (HA) crystals in joints is closely associated with OA and other arthropathies, but ...

متن کامل

Mir-155 is overexpressed in systemic sclerosis fibroblasts and is required for NLRP3 inflammasome-mediated collagen synthesis during fibrosis

BACKGROUND Despite the important role that microRNAs (miRNAs) play in immunity and inflammation, their involvement in systemic sclerosis (SSc) remains poorly characterized. miRNA-155 (miR-155) plays a role in pulmonary fibrosis and its expression can be induced with interleukin (IL)-1β. SSc fibroblasts have activated inflammasomes that are integrally involved in mediating the myofibroblast phen...

متن کامل

Targeting ASC in NLRP3 inflammasome by caffeic acid phenethyl ester: a novel strategy to treat acute gout

Gouty arthritis is caused by the deposition of uric acid crystals, which induce the activation of NOD-like receptor family, pyrin domain containing 3(NLRP3) inflammasome. The NLRP3 inflammasome, composed of NLRP3, the adaptor protein ASC, and caspase-1, is closely linked to the pathogenesis of various metabolic diseases including gouty arthritis. We investigated whether an orally administrable ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Mediators of inflammation

دوره 2016  شماره 

صفحات  -

تاریخ انتشار 2016