Mycoplasma meleagridis-induced lesions in the tarsometatarsal joints of turkey embryos.

Mycoplasma meleagridis (MM) has the ability to cause bone deformity in turkey poults. However, few pathological lesions have been described and no evidence of MM-induced damage to the bones has been shown. In this study, 17-day-old turkey embryos were inoculated with MM into the allantoic cavity. On the 27th day, eight of the 22 embryos presented with curved toes. Scanning electron microscopy of the tarsometatarsal joints showed fissures in the cartilage. Histological sections of the joints revealed only the infiltration of cells with eosinophilic granules. Immunohistochemical staining (IHS) showed the presence of MM in the aggregates of the bone marrow cells and the cells with eosinophilic granules. Some of these cells were harvested by laser capture microdissection (LCM), lysed, and used as template DNA. With a pair of MM-specific primers in a conventional polymerase chain reaction (PCR), a gene product was amplified, and it comigrated with the MM DNA, which indicates that these captured cells contained MM DNA. Thus, this research shows that inoculation of MM into the turkey embryos produced joint lesions and caused cellular infiltration within the bones.

Effect of phospholipase A2 inhibitory peptide on inflammatory arthritis in a TNF transgenic mouse model: a time-course ultrastructural study.

We evaluated the therapeutic effect of secretory phospholipase A2 (sPLA2)-inhibitory peptide at a cellular level on joint erosion, cartilage destruction, and synovitis in the human tumor necrosis factor (TNF) transgenic mouse model of arthritis. Tg197 mice (N = 18) or wild-type (N = 10) mice at 4 weeks of age were given intraperitoneal doses (7.5 mg/kg) of a selective sPLA2 inhibitory peptide, P-NT.II, or a scrambled P-NT.II (negative control), three times a week for 4 weeks. Untreated Tg197 mice (N = 10) were included as controls. Pathogenesis was monitored weekly for 4 weeks by use of an arthritis score and histologic examinations. Histopathologic analysis revealed a significant reduction after P-NT.II treatment in synovitis, bone erosion, and cartilage destruction in particular. Conspicuous ultrastructural alterations seen in articular chondrocytes (vacuolated cytoplasm and loss of nuclei) and synoviocytes (disintegrating nuclei and vacuoles, synovial adhesions) of untreated or scrambled-P-NT.II-treated Tg197 mice were absent in the P-NT.II-treated Tg197 group. Histologic scoring and ultrastructural evidence suggest that the chondrocyte appears to be the target cell mainly protected by the peptide during arthritis progression in the TNF transgenic mouse model. This is the first time ultrastructural evaluation of this model has been presented. High levels of circulating sPLA2 detected in untreated Tg197 mice at age 8 weeks of age were reduced to basal levels by the peptide treatment. Attenuation of lipopolysaccharide- and TNF-induced release of prostaglandin E2 from cultured macrophage cells by P-NT.II suggests that the peptide may influence the prostaglandin-mediated inflammatory response in rheumatoid arthritis by limiting the bioavailability of arachidonic acid through sPLA2 inhibition.

Type II collagen-induced arthritis. Studies with purified anticollagen immunoglobulin.

Immunization of rats with native bovine type II collagen results in a polyarthritis by day 21 in approximately 40% of the rats. Sera of these rats contained anticollagen IgG, principally IgG2a. Small amounts of IgG2b were also detected, but IgG1 and IgG2c were absent. By enzyme-linked immunosorbent assay, the paw tissue of these polyarthritic rats was shown to contain anticollagen IgG, the principal subclass being IgG2a, with minor amounts of IgG2b. Immunofluorescence examination of the paws from polyarthritic rats demonstrated deposition of both IgG and C3 on the articular surface. Passive transfer of disease was accomplished by injection of affinity-purified anticollagen immunoglobulin into naive recipients; paw swelling and histopathologic changes were detected 24 hours after transfer, and by immunofluorescence techniques IgG and C3 deposits were demonstrable on the articular cartilage. On passive transfer, neutrophils invaded the joint space and became juxtaposed to the surface of the articular cartilage. Passive transfer of the disease with anticollagen immunoglobulin was unsuccessful after rats were decomplemented with cobra venom factor; immunofluorescence demonstrated IgG but not C3 on the articular cartilage of these decomplemented rats. In rats decomplemented with cobra venom factor, neutrophils did not accumulate in the joint and erosion of articular cartilage was not detected.