Experimental animal models of rheumatoid arthritis.

1. Experimental animal models of
rheumatoid arthritis
Lab 2 Group 1 ID: 17026 : 17040 & 17327

2. Pathogenesis of Rheumatoid
Arthritis.
• Phase one :
Initiation phase due to non-specific inflammation
• Phase two :
Amplification phase due to T-Cell activation
• Phase three :
Chronic inflammatory phase with tissue injury
resulting from the cytokines ,IL 1,TNF-alfa and IL-6.

4. Antigen
induced
arthritis Proteoglycan
induced
arthritis
(G6PI)
Streptococcal
cell wall
induced
arthritis
(SCWIA)
Cartilage
Oligomeric
matrix
Protein
(COMP)
Induced
arthritis
Collagen
induced
arthritis
(CIA)

5. Streptococcal cell wall induced
arthritis (SCWIA)
• Streptococcus pyogenes produce a peptidoglycan-
polysaccharide (PG-PS) polymer, which is found to possess
high inflammatory activity and it also has the capacity to
induce arthritis in rats.
• An intraperitoneal injection of PG-PS 10 S induces
polyarticular arthritis in female Lewis rats results in acute
inflammation response and swelling of the joints. During
the first five days, the joint inflammation progresses and it
is followed by a period of respite, after which impetuous
reactivation occurs, resulting in chronic arthritis.

6. Streptococcal cell wall induced
arthritis (SCWIA)
• This model provides an opportunity to study the early and
more chronic phases of arthritis20. The initial response,
which was observed is not T cell dependent. There is
involvement of monocytes in both the acute phase and
further development of arthritis. During the chronic phase,
the severity of arthritis can be correlated with the
activation status of T cells, B cells and monocytes.
• There is also an interrelation between the degree of
inflammation and the production of TNF-a, IL-6, IL-122.
Some of the hallmarks of this model in similarity to human
RA include synovial hyperplasia, infiltration of inflammatory
cells, involvement of symmetric joints and relapsing
inflammation.