Mycoplasma synoviae cell invasion: Elucidation of the Mycoplasma pathogenesis in chicken

Buim, M. R.; Buzinhani, Melissa; Yamaguti, Maurício; Oliveira, Renata Cristina Gobbi de; Mettifogo, Elena; Ueno, Priscila M.; Timenetsky, Jorge; Santelli, Gláucia M.M.; Ferreira, Antônio José Piantino

doi:10.1016/j.cimid.2009.11.001

Cited by 21 publications

(18 citation statements)

References 21 publications

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“…The invasion at 4 h post infection was quite low (0.032% ± 0.01) and thereafter increased exponentially with highest rates witnessed at 24 h post infection (2.28% ± 0.19). Such long infection periods and/or comparable invasion frequencies have earlier been reported for many bacterial pathogens, including mycoplasmas, which were predominantly known to be extracellular but were subsequently shown to have alternative intracellular lifestyle ( Martin and Mohr, 2000; Dusanic et al, 2009; Marques et al, 2010; Buim et al, 2011; Hopfe et al, 2013; Lamberti et al, 2013 ). The percentage invasion frequency differed slightly for the three cell types.…”

Section: Resultssupporting

confidence: 59%

In vitro and in vivo cell invasion and systemic spreading of Mycoplasma agalactiae in the sheep infection model

Hegde¹,

Hegde²,

Spergser³

et al. 2014

International Journal of Medical Microbiology

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Generally regarded as extracellular pathogens, molecular mechanisms of mycoplasma persistence, chronicity and disease spread are largely unknown. Mycoplasma agalactiae, an economically important pathogen of small ruminants, causes chronic infections that are difficult to eradicate. Animals continue to shed the agent for several months and even years after the initial infection, in spite of long antibiotic treatment. However, little is known about the strategies that M. agalactiae employs to survive and spread within an immunocompetent host to cause chronic disease. Here, we demonstrate for the first time its ability to invade cultured human (HeLa) and ruminant (BEND and BLF) host cells. Presence of intracellular mycoplasmas is clearly substantiated using differential immunofluorescence technique and quantitative gentamicin invasion assays. Internalized M. agalactiae could survive and exit the cells in a viable state to repopulate the extracellular environment after complete removal of extracellular bacteria with gentamicin. Furthermore, an experimental sheep intramammary infection was carried out to evaluate its systemic spread to organs and host niches distant from the site of initial infection. Positive results obtained via PCR, culture and immunohistochemistry, especially the latter depicting the presence of M. agalactiae in the cytoplasm of mammary duct epithelium and macrophages, clearly provide the first formal proof of M. agalactiae's capability to translocate across the mammary epithelium and systemically disseminate to distant inner organs. Altogether, the findings of these in vitro and in vivo studies indicate that M. agalactiae is capable of entering host cells and this might be the strategy that it employs at a population level to ward off the host immune response and antibiotic action, and to disseminate to new and safer niches to later egress and once again proliferate upon the return of favorable conditions to cause persistent chronic infections.

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Section: Resultssupporting

confidence: 59%

In vitro and in vivo cell invasion and systemic spreading of Mycoplasma agalactiae in the sheep infection model

Hegde¹,

Hegde²,

Spergser³

et al. 2014

International Journal of Medical Microbiology

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“…Intracellularly, M. bovis appeared in clusters with no apparent localization in specific cellular compartments as it was observed for M. gallisepticum in HeLa-229 cells and chicken embryo fibroblasts (CEF) by double immunofluorescence microscopy [ 20 ] or M. pneumoniae in normal human bronchial epithelial cells by immunofluorescence microscopy [ 57 ]. M. synoviae is spread throughout the cytoplasm but is also observed in clusters around the nuclei in the human epithelial cell line HEp-2 as investigated by confocal laser scanning microscopy [ 58 ] and M. genitalium strains G37 and 1019 V are found peri-, and intranuclearly in HeLa and EM42 cells using immunofluorescence and confocal microscopy [ 59 ]. M. bovis strain Mb1, invading different populations of PBMCs, displayed different intracellular patterns depending on the individual cell population or the time of infection [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Invasion and persistence of Mycoplasma bovis in embryonic calf turbinate cells

Bürki

Gaschen

Stoffel

et al. 2015

Vet Res

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Mycoplasma bovis is a wall-less bacterium causing bovine mycoplasmosis, a disease showing a broad range of clinical manifestations in cattle. It leads to enormous economic losses to the beef and dairy industries. Antibiotic treatments are not efficacious and currently no efficient vaccine is available. Moreover, mechanisms of pathogenicity of this bacterium are not clear, as few virulence attributes are known. Microscopic observations of necropsy material suggest the possibility of an intracellular stage of M. bovis. We used a combination of a gentamicin protection assay, a variety of chemical treatments to block mycoplasmas entry in eukaryotic cells, and fluorescence and transmission electron microscopy to investigate the intracellular life of M. bovis in calf turbinate cells. Our findings indicate that M. bovis invades and persists in primary embryonic calf turbinate cells. Moreover, M. bovis can multiply within these cells. The intracellular phase of M. bovis may represent a protective niche for this pathogen and contribute to its escape from the host’s immune defense as well as avoidance of antimicrobial agents.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-015-0194-z) contains supplementary material, which is available to authorized users.

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“…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.…”

Section: Il-8mentioning

confidence: 99%

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

et al. 2020

Front. Microbiol.

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High-Throughout Analysis of MS-Infected CSF involved in the pathogenesis of MS-induced arthritis in chickens. To our knowledge, this is the first integrated analysis on the mechanism of CSF-MS interactions that combined transcriptomic and proteomic technologies. In this study, many key candidate genes and their protein products related to MS-induced infectious synovitis and arthritis were identified.

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Mycoplasma synoviae cell invasion: Elucidation of the Mycoplasma pathogenesis in chicken

Cited by 21 publications

References 21 publications

In vitro and in vivo cell invasion and systemic spreading of Mycoplasma agalactiae in the sheep infection model

In vitro and in vivo cell invasion and systemic spreading of Mycoplasma agalactiae in the sheep infection model

Invasion and persistence of Mycoplasma bovis in embryonic calf turbinate cells

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

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