How to Model Rheumatoid Arthritis in Animals: From Rodents to Non-Human Primates

Zhao, Ting; Xie, Zhaohu; Xi, Yujiang; Liu, Li; Li, Zhaofu; Qin, Dongdong

doi:10.3389/fimmu.2022.887460

Cited by 10 publications

(30 citation statements)

References 65 publications

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“…Poultry models offer closer uric acid metabolism pathways to humans and some clinical symptom reflection, but significant limitations arise from genomic differences and specialized feeding requirements. In comparison, non-human primates demonstrate superior surface, construct, and predictive validity for GN ( 87 ). Although literature lacks established models, their closer metabolic and genomic relationship to humans holds promise for drug development.…”

Section: Discussionmentioning

confidence: 93%

Models of gouty nephropathy: exploring disease mechanisms and identifying potential therapeutic targets

Wang,

Zhang,

Shen

et al. 2024

Front. Med.

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Gouty nephropathy (GN) is a metabolic disease with persistently elevated blood uric acid levels. The main manifestations of GN are crystalline kidney stones, chronic interstitial nephritis, and renal fibrosis. Understanding the mechanism of the occurrence and development of GN is crucial to the development of new drugs for prevention and treatment of GN. Currently, most studies exploring the pathogenesis of GN are primarily based on animal and cell models. Numerous studies have shown that inflammation, oxidative stress, and programmed cell death mediated by uric acid and sodium urate are involved in the pathogenesis of GN. In this article, we first review the mechanisms underlying the abnormal intrinsic immune activation and programmed cell death in GN and then describe the characteristics and methods used to develop animal and cell models of GN caused by elevated uric acid and deposited sodium urate crystals. Finally, we propose potential animal models for GN caused by abnormally high uric acid levels, thereby provide a reference for further investigating the methods and mechanisms of GN and developing better prevention and treatment strategies.

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Section: Discussionmentioning

confidence: 93%

Models of gouty nephropathy: exploring disease mechanisms and identifying potential therapeutic targets

Wang,

Zhang,

Shen

et al. 2024

Front. Med.

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“…The main effector cells appear to be neutrophils and macrophages, which are activated by immune complexes formed in the joints via binding of CII antibodies to cartilage surfaces [ 23 ]. Typical pathological changes observed in RA, such as synovitis, pannus formation, and cartilage and bone destruction, are observed in the joints of animals with CAIA [ 24 , 25 ]. Although the cytokines involved in the pathogenesis of CAIA have not been studied in detail, the involvement of IL-1β, IL-6, and TNF is anticipated [ 24 , 26 ].…”

Section: Murine Models Of Rheumatoid Arthritismentioning

confidence: 99%

The use of animal models in rheumatoid arthritis research

Jeong¹,

Yoo²

2023

J Yeungnam Med Sci

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The pathological hallmark of rheumatoid arthritis (RA) is a synovial pannus that comprises proliferating and invasive fibroblast-like synoviocytes, infiltrating inflammatory cells, and an associated neoangiogenic response. Animal models have been established to study these pathological features of human RA. Spontaneous and induced animal models of RA primarily reflect inflammatory aspects of the disease. Among various induced animal models, collagen-induced arthritis (CIA) and collagen antibody-induced arthritis (CAIA) models are widely used to study the pathogenesis of RA. Improved transplantation techniques for severe combined immunodeficiency (SCID) mouse models of RA can be used to evaluate the effectiveness of potential therapeutics in human tissues and cells. This review provides basic information on various animal models of RA, including CIA and CAIA. In addition, we describe a SCID mouse coimplantation model that can measure the long-distance migration of human RA synoviocytes and cartilage destruction induced by these cells.

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“…Animal models of rheumatoid arthritis (RA) were intensively investigated by several groups in the neuroimmune context. Most RA models are performed in rodents, although there are also valid models in nonhuman primates [98]. There are several spontaneous (mice with susceptible genetic backgrounds: K/BxN, SKG, IL1ra deficient, TNF transgenic) and induced (collagen-induced arthritis [CIA], adjuvant-induced arthritis [AA], DTHA, pristane-induced arthritis, ACPA-induced arthritis, CAIA) animal models for RA; however, the most widely used and studied in the neuroimmune context are CIA and AA (Table 4).…”

Section: Effects Of Sns In Models Of Chronic Inflammationmentioning

confidence: 99%

“…CIA is induced by immunizing susceptible mice (mostly DBA1/J) at the base of their tails with bovine type 2 collagen mixed with complete Freund´s adjuvant. CIA is regarded to closely resemble human disease due to chronicity, antibody dependence and arthritis morphology as opposed to AA [98].…”

Section: Effects Of Sns In Models Of Chronic Inflammationmentioning

confidence: 99%

Chronic Effects of the Sympathetic Nervous System in Inflammatory Models

Pongratz¹,

Straub²

2023

Neuroimmunomodulation

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The immune system is embedded in a network of regulatory systems to keep homeostasis in case of an immunologic challenge. Neuroendocrine immunologic research has revealed several aspects of these interactions over the past decades, e.g., between the autonomic nervous system and the immune system. This review will focus on evidence revealing the role of the sympathetic nervous system (SNS) in chronic inflammation, like colitis, multiple sclerosis, systemic sclerosis, lupus erythematodes, and arthritis with a focus on animal models supported by human data. A theory of the contribution of the SNS in chronic inflammation will be presented that spans these disease entities. One major finding is the biphasic nature of the sympathetic contribution to inflammation, with proinflammatory effects until the point of disease outbreak and mainly anti-inflammatory influence thereafter. Since sympathetic nerve fibers are lost from sites of inflammation during inflammation, local cells and immune cells achieve the capability to endogenously produce catecholamines to fine-tune the inflammatory response independent of brain control. On a systemic level, it has been shown across models that the SNS is activated in inflammation as opposed to the parasympathetic nervous system. Permanent overactivity of the SNS contributes to many of the known disease sequelae. One goal of neuroendocrine immune research is defining new therapeutic targets. In this respect, it will be discussed that at least in arthritis, it might be beneficial to support β-adrenergic and inhibit α-adrenergic activity besides restoring autonomic balance. Overall, in the clinical setting, we now need controlled interventional studies to successfully translate the theoretical knowledge into benefits for patients.

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How to Model Rheumatoid Arthritis in Animals: From Rodents to Non-Human Primates

Cited by 10 publications

References 65 publications

Models of gouty nephropathy: exploring disease mechanisms and identifying potential therapeutic targets

Models of gouty nephropathy: exploring disease mechanisms and identifying potential therapeutic targets

The use of animal models in rheumatoid arthritis research

Chronic Effects of the Sympathetic Nervous System in Inflammatory Models

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