Mycoplasma synoviae induces upregulation of apoptotic genes, secretion of nitric oxide and appearance of an apoptotic phenotype in infected chicken chondrocytes

摘要: The role of chondrocytes in the development infectious arthritis is not well understood. Several examples mycoplasma-induced animals indicate that come into direct contact with bacteria. objective this study was to analyze interaction an arthrogenic Mycoplasma synoviae strain WVU 1853 chicken chondrocytes. We found M. significantly reduces chondrocyte respiration. This accompanied by alterations morphology, namely cell shrinkage and cytoplasm condensation, as nuclear condensation formation plasma membrane invaginations containing material, which appeared cleave off surface. In concordance these apoptosis-like events chondrocytes, transcription increased several pro-apoptotic genes. Twenty-four hours after infection, strong upregulation assayed NOS2, Mapk11, CASP8 Casp3 72 h incubation induced AIFM1, NFκB1, htrA3 BCL2. NOS2 remained upregulated, but ceased for Mapk11 Increased production nitric oxide also confirmed supernates. data suggests infected die apoptosis involving oxide, caspase 3 activation mitochondrial inactivation. results show first time mycoplasmas could cause apoptosis. contribute tissue destruction influence arthritic conditions. Hence, gives new insights mycoplasma infection on biology chickens potentially humans.