Phenotypic Characterization ofMycoplasma synoviaeInduced Changes in the Metabolic and Sensitivity Profile ofIn VitroInfected Chicken Chondrocytes

Abstract

In infectious synovitis caused by Mycoplasma synoviae chicken chondrocytes (CCH) may come into direct contact with these bacteria that are also capable of invading CCH in vitro. In this study, phenotype microarrays were used to evaluate the influence of Mycoplasma synoviae on the global metabolic activity of CCH. Therefore, CCH were cultured in the presence of 504 individual compounds, spotted in wells of 11 phenotype microarrays for eukaryotic cells, and exposed to Mycoplasma synoviae membranes or viable Mycoplasma synoviae. Metabolic activity and sensitivity of normal cells versus infected cells were evaluated. Metabolic profiles of CCH treated with viable Mycoplasma synoviae or its membranes were significantly different from those of CCH alone. CCH treated with Mycoplasma synoviae membranes were able to use 48 carbon/nitrogen sources not used by CCH alone. Treatment also influenced ion uptake in CCH and intensified the sensitivity to 13 hormones, 5 immune mediators, and 29 cytotoxic chemicals. CCH were even more sensitive to hormones/immune mediators when exposed to viable Mycoplasma synoviae. Our results indicate that exposure to Mycoplasma synoviae or its membranes induces a wide range of metabolic and sensitivity modifications in CCH that can contribute to pathological processes in the development of infectious synovitis.

Integrated Transcriptomic and Proteomic Analyses of the Interaction Between Chicken Synovial Fibroblasts and Mycoplasma synoviae

“…Nitric oxide synthase 2 395807 3.393184476 NA Lavric et al, 2007;Lavric et al, 2008; Narat et al, 1998;Lavric et al, 2007;Dusanic et al, 2014 Il-6 Interleukin 6 395337 8.876096951 2.033158667…”

“…Interleukin 8 396495 9.695048495 2.287767778 Narat et al, 1998;Bodolay et al, 2002;Lavric et al, 2007;Dusanic et al, 2014 Pro are key cells that drive pathological processes (Ospelt et al, 2004;Bartok and Firestein, 2010;Carmona-Rivera et al, 2017;Falconer et al, 2018). SF can release proinflammatory mediators and chemotactic factors that activate complement factors, resulting in inflammation (Bodolay et al, 2002;Mathew and Ravindran, 2014;Yoshitomi, 2019).…”

“…The application of high-throughput methods on MS-induced arthritis could lead to the discovery of pathogenesis-related genes and proteins. However, high-throughput methods have not been applied in most studies of host-MS interactions, with the exception of two studies that utilized an avian macrophage microarray/avian innate immunity microarray (Lavric et al, 2008) and a phenotype microarray (Dusanic et al, 2014). To uncover the molecular mechanisms of MS-induced arthritis, primary CSF were prepared by the explanted tissue culture method in this study (Supplementary Figure S1).…”

“…Recent studies demonstrated that MS-invaded host cells incubated and altered the gene expression of these cells after 24, 48, or 72 h (Dusanic et al, 2009;Buim et al, 2011;Dusanic et al, 2012Dusanic et al, , 2014Cizelj et al, 2016). Combining these studies and comprehensive analysis, we employed highthroughput methods to analyze the gene expression of MSinfected CSF 48 hpi.…”

“…Addis et al (2011) utilized a proteomic approach to investigate the impact of M. agalactiae infection on mammary epithelium. Another study employed phenotype microarrays to investigate the influence of MS on the global metabolic activity of chicken chondrocytes (CCH) (Dusanic et al, 2014). A separate study performed a quantitative real-time polymerase chain reaction (qRT-PCR) assay of gene expression in an in vitro co-culture of MS and CCH (Cizelj et al, 2016).…”