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Using a cocktail or anti-type II collagen antibodies induces a synchronized model of arthritis in just a few days.
The collagen-induced arthritis (CIA) model is mediated by autoantibodies that bind to a particular region of type II collagen (CII) and complement. Initial symptoms of inflammation occur at approximately day 21 with the model requiring 6-8 weeks to complete. These time requirements, along with variable disease onset, have caused researchers to look for more efficient and cost effective alternatives. MD Bioproducts ArthritoMab• Antibody Cocktail (Cat. no. CIA-MAB) consists of four monoclonal antibodies to CII that bind to the well-defined epitopes C1, J1, D3, and U1. These epitopes are spread across the entire CII region, are found in mice immunized with CII and developing arthritis, and encourage better immune complex formation on the cartilage surface or in the synovium (1). These complexes can then activate, complement, and induce inflammation by both the classical and alternative pathways. Monocytes in the joint are also activated by these complexes via Fc receptors releasing pro-inflammatory cytokines, (i.e., TNF-α and IL-1β), which recruit neutrophils and macrophages.
Monoclonal Antibody Induced Arthritis: a shorter, more synchronized alternative to the classic CIA model
Collagen-induced arthritis (CIA) in mice is widely used as an experimental model for rheumatoid arthritis. Initial symptoms of inflammation in the CIA model occur at approximately day 21-24 with the model requiring 6-8 weeks to complete. The induction of the disease is typically at 80% of the animals and varies from laboratory to laboratory and with the use of different collagen sources. The disease symptoms also appear at slightly different times in different animals, making therapeutic administration protocols more demanding technically. With the long study length, significant amounts of compounds are required to be prepared for use over the study duration. Furthermore, the lengthy study period also requires increased number of measurements and scoring periods, increasing the cost of the study further. Theses points illustrate some of the key issues in running a typical CIA model. The monoclonal antibody induced arthritis model (mAb-induced RA, AIA or CAIA) is ideal for rapidly screening and evaluating anti-inflammatory therapeutic agents providing more information in a shorter amount of time. The flexibility of the system means it is applicable to the wide range of transgenic strain bred on the C57Bl background. It is also relevant for studying inflammatory mediators such as cytokines, chemokines, matrix metalloproteinases and other factors such as the role of bacterial flora and their by-products in triggering and exacerbating arthritis.
View the article published in 2008 Biotechniques of the CAIA model using ArthritoMab™ Antibody Cocktail
Matrix metalloproteinases (MMPs) comprise a family of secreted and membrane-bound endopeptides that hydrolyze extracellular matrix proteins (ECM). Based on their preferred substrates and structural features, MMPs can be divided into collagenases, gelatinases, stromelysins, matrilysins and membrane-type matrix metalloproteinases (MT-MMP). MMp mediated ECM degradation affects processes such as connective tissue remodeling, cell migration and cell micro-environment regulation. MMPs further affect cellular behavior by modulatin the activities of cytokines, growth factors cell surface receptors and other MMPs. In addtion to their normal function in developmental and repair processes, inappropriate MMP activity also participates in diseases processes including arthritis and cancer.
An ELISA to Measure Proteolytic Degradation of Aggrecan: Hallmark in the pathology of Arthritis.
Aggrecan is a large aggregating proteoglycan of articular cartilage (1), making up 10% of the dry weight. It is responsible for hydrating cartilage giving it compressibility and resilience during joint loading, thereby playing a major role in the normal function of cartilage. Depletion of glycosaminoglycan bearing aggrecan fragments from articular cartilage is one of the earliest events in cartilage destruction.