Characteristics of synovial fluid effusion in collagen-induced arthritis (CIA) in the DA rat; a comparison of histology and antibody reactivities in an experimental chronic arthritis model and rheumatoid arthritis (RA)

Abstract

SUMMARYWe have characterized the cellular content and some antibody reactivities in synovial fluid (SF) from DA rats with CIA. Since CIA is widely used as a model for RA, in which many studies concerning immune responses are performed on SF samples, we considered it important to describe the local, disease-causing immune reactions in CIA. At the peak of disease (day 22 after immunization), the major cell population in CIA SF was granulocytes (72%), but macrophages (17 . 9%), plasma cells (2 . 6%) and lymphocytes (7 . 7%) were also present. The CIA synovial membrane (SM) obtained at the same time was mainly infiltrated by monocytes, with granulocytes, lymphocytes and plasma cells also present. Cell populations in blood did not differ between arthritic and normal DA rats. Equally, high anti-collagen type II (CII) and rheumatoid factor (RF) levels could be detected both in SF and in sera. Notably, RF levels were also increased in normal DA rats. Moderate levels of anti-heat shock protein 65 kD (hsp) antibodies were recorded systemically in both normal and diseased animals. In conclusion, the cellular composition in SF and in SM are similar in rat CIA and in RA. The morphological differences between SF and SM that are characteristic for RA could also be demonstrated in CIA. The antibody data indicate systemic production of anti-CII and anti-hsp antibodies as well as RF, but they give no support for local production of these antibodies in the joints, which is the case in RA.

Leukotriene-A4-Hydrolase and Basic Aminopeptidase Activities Are Related with Collagen-Induced Arthritis in a Compartment-Dependent Manner

“…These data agree with the differential detection of serum TNF-α levels and histopathological alterations of the tibio-tarsal joint in the CII treated animals that develop severe edema (CIA-arthritic), which can be thus confidentially distinguished from CIA-resistant (without edema) [28,29]. Based on the macroscopic classification of edema formation, preconized by Erlandsson Harris et al [39], all arthritic animals selected here had the maximum score in hind paws. 10% of CII treated animals were discarded because they did not reach this level of arthritis.…”

The Involvement of Heat-Shock Proteins in the Pathogenesis of Autoimmune Arthritis: A Critical Appraisal

“…Heat-shock proteins (HSPs) 4-7 (Table 1) are implicated in the pathogenesis of experimental arthritis in rodents 8-15 as well as human RA 16-18 . The T cells and antibodies from arthritic animals and RA patients are directed against different HSPs 15,19-23 . Various HSPs share a common characteristic of inducibility by heat-shock or other stressful stimuli, and these HSPs can be categorized into 9 protein families (Table 1).…”

Antigen-Specific Tolerogenic Dendritic Cells Ameliorate the Severity of Murine Collagen-Induced Arthritis

“…Collagen-induced arthritis (CIA) is a well-established mouse model of experimental arthritis with many of the pathological characteristics of human RA [ 15 ]. We hypothesized that type II collagen (CII)–pulsed tolDCs would induce antigen-specific immune tolerance in autoimmune disorders (AIDs) and would ameliorate arthritis progression.…”