Interaction of polymorphonuclear leukocytes with immune complexes trapped in joint collagenous tissues

Abstract

The present experiments were designed to investigate in vitro interactions between polymorphonuclear leukocytes (PMN) and rabbit joint collagenous tissues containing trapped immune complexes. Articular cartilages and menisci from antigen-injected and control joints were incubated with normal PMN isolated from rabbit peritoneal exudates or blood. After incubation of cartilage and menisci from antigen-injected joints with PMN, large numbers of PMN became attached to the articular surface. In areas of superficial erosion, the PMN invaded the tissue several cell diameters below the articular surface. Through immunoelectron microscopy, degranulated PMN were observed in scattered areas to phagocytose amorphous material containing rabbit Ig. Following addition of PMN to control tissues, only a few PMN became attached to the articular surface. When tissues from monosodium urate-injected joints were incubated with PMN, these cells were found attached to the surface in moderate numbers, but invasion into the tissues was not seen. These studies indicate that immune complexes trapped in joint collagenous tissues may lead to enhanced release of lysosomal hydrolases.In rabbits previously immunized to a soluble antigen, intraarticular injection of the antigen results in the development of a chronic arthritis and the formation of immune complexes (IC) that are trapped within the joint collagenous tissues and persist in the inflamed joint for long periods of time (1-3). IC have also been found in the articular cartilage and menisci obtained from a majority of patients with rheumatoid arthritis (4.5). The role of the trapped IC in the maintenance of acute and chronic inflammation both in the animal model and the rheumatoid joint is unknown, but recent work from this laboratory (6) suggests that the trapped complexes are able to activate the complement system and generate mediators of inflammation. Moreover, the trapped complexes induced the formation of pannuslike inflammatory capsules in immune complex-containing menisci transferred to the suprapatellar pouches of previously immunized rabbits ( 6 ) .Henson (7,8) and Hawkins (9) have previously shown that 1C trapped on artificial membranes were able to induce the release of lysosomal hydrolases from polymorphonuclear leukocytes (PMN) permitted to interact with the 1C irreversibly trapped on such surfaces. The release of lysosomal enzymes was attributed to "re-

Rheumatoid synovial fibroblast adhesion to human articular cartilage

“…The observations that treatment of cartilage with supernatants obtained from activated neutrophils increases synovial fibroblast adherence and that the enhanced adherence is inhibited when the supernatant is treated with EGTA and DFP suggest that neutrophil proteases are at least in part responsible for the observed enhancement of fibroblast adherence. These results are consistent with findings of previous studies demonstrating that when neutrophils are exposed to cartilage from patients with RA, there is degradation of subjacent cartilage (18,19) and that neutrophils in synovial fluid interacting with surface-adherent IgG can degrade cartilage (20). Immunohistologic studies demonstrating neutrophil proteases on the surface of rheumatoid articular cartilage (2 1) provide further evidence that this process may be operative in vivo.…”

Reduction of chemokine levels and leukocyte traffic to joints by tumor necrosis factor α blockade in patients with rheumatoid arthritis

“…RA pannus, the site of characteristic periarticular erosions, contains relatively few neutrophils, but these cells have been identified at the cartilage-pannus junction (30)(31)(32)(33). Immune complexes, including rheumatoid factor and antibodies to type II collagen, are embedded in the superficial layers of RA cartilage (34)(35)(36)(37). Such complexes may effectively act as cartilage opsonins (36), allowing neutrophils to adhere and discharge their contents directly against cartilage in a process termed "frustrated phagocytosis" (29).…”

Immunohistochemical detection and immunochemical analysis of type II collagen degradation in human normal, rheumatoid, and osteoarthritic articular cartilages and in explants of bovine articular cartilage cultured with interleukin 1.

“…This collagen degradation may be caused by proteolytic enzymes originating from the synovial fluid which are capable of degrading collagen. Obvious candidates are the collagen-degrading proteases, elastase and cathepsin G (40, 42), which can be released by polymorphonuclear leukocytes upon attachment to articular cartilage which results in the degradation of the more superficial articular cartilage (43,44). In one specimen (K.E.…”