Effect of Mycoplasma arthritidis superantigen on enzymatically induced arthritis in mice
Autor: | N. Hozumi, P. A. Quinn, R. A. Kandel, Cynthia A. Chambers, T. F. Cruz, H. Sustackova |
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Jazyk: | angličtina |
Rok vydání: | 1995 |
Předmět: |
musculoskeletal diseases
Lymphocyte medicine.medical_treatment Receptors Antigen T-Cell alpha-beta Immunology Intraperitoneal injection Arthritis Inflammation Biology Lymphocyte Activation Mice Immune system Mycoplasma medicine Superantigen Immunology and Allergy Animals Collagenases Cells Cultured Antigens Bacterial Mice Inbred BALB C Superantigens Cartilage fungi medicine.disease Flow Cytometry medicine.anatomical_structure Collagenase Female medicine.symptom Mitogens medicine.drug Research Article |
Popis: | SUMMARY The objective of this study was to examine the effect of the stimulation of the immune system with Mycoplasma arthritidis superantigen (MAS) on joint inflammation and cartilage destruction. MAS was administered either alone or combined with a model of degenerative arthritis induced by intraarticular injection of collagenase enzyme. Intraperitoneal injection of MAS resulted in activation of peripheral lymphocytes in BALB/c mice, as shown by a proliferative response of splenocytes isolated from MAS-treated animals to IL-2-containing supernatant. Intraperitoneal or intraarticular administration of MAS alone at concentrations maximally activating lymphocytes had no detectable effect on joints. Intraarticular injection of collagenase resulted in some infiltration of inflammatory cells into the joints, hyperplasia and hypertrophy of synovial lining, pannus formation and surface loss of proteoglycans 7 days following the injection. At 21 days, the animals showed almost total loss of cartilage and minimal or no inflammation. Animals receiving MAS in addition to collagenase treatment showed similar changes in the joints. These data have demonstrated that activation of the immune system with MAS in vivo does not increase joint inflammation or cartilage degradation in enzymatically induced arthritis. |
Databáze: | OpenAIRE |
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