Detection of antibodies against the Mycoplasma bovis glyceraldehyde-3-phosphate dehydrogenase protein in beef cattle

Perez-Casal, José; Prysliak, Tracy

doi:10.1016/j.micpath.2007.05.009

Cited by 41 publications

(28 citation statements)

References 24 publications

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“…All experiments were conducted by using M. bovis strain Mb1, which was previously isolated from the synovial fluid of a calf exhibiting signs of arthritis (25). Cultures were grown in modified Hayflick's medium at 37°C in a 5% CO 2 atmosphere.…”

Section: Methodsmentioning

confidence: 99%

In VitroInfection of Bovine Monocytes with Mycoplasma bovis Delays Apoptosis and Suppresses Production of Gamma Interferon and Tumor Necrosis Factor Alpha but Not Interleukin-10

et al. 2014

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bMycoplasma bovis is one of the major causative pathogens of bovine respiratory complex disease (BRD), which is characterized by enzootic pneumonia, mastitis, pleuritis, and polyarthritis. M. bovis enters and colonizes bovine respiratory epithelial cells through inhalation of aerosol from contaminated air. The nature of the interaction between M. bovis and the bovine innate immune system is not well understood. We hypothesized that M. bovis invades blood monocytes and regulates cellular function to support its persistence and systemic dissemination. We used bovine-specific peptide kinome arrays to identify cellular signaling pathways that could be relevant to M. bovis-monocyte interactions in vitro. We validated these pathways using functional, protein, and gene expression assays. Here, we show that infection of bovine blood monocytes with M. bovis delays spontaneous or tumor necrosis factor alpha (TNF-␣)/staurosporine-driven apoptosis, activates the NF-B p65 subunit, and inhibits caspase-9 activity. We also report that M. bovis-infected bovine monocytes do not produce gamma interferon (IFN-␥) and TNF-␣, although the level of production of interleukin-10 (IL-10) is elevated. Our findings suggest that M. bovis takes over the cellular machinery of bovine monocytes to prolong bacterial survival and to possibly facilitate subsequent systemic distribution.

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Section: Methodsmentioning

confidence: 99%

In VitroInfection of Bovine Monocytes with Mycoplasma bovis Delays Apoptosis and Suppresses Production of Gamma Interferon and Tumor Necrosis Factor Alpha but Not Interleukin-10

et al. 2014

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“…M. bovis Mb1 was used for all experiments and was previously isolated from synovial joint fluid of a calf showing signs of arthritis (23). Cultures containing M. bovis Mb1 were grown in modified Hayflick medium at 37°C in a 5% CO 2 atmosphere.…”

Section: Methodsmentioning

confidence: 99%

Invasion of Bovine Peripheral Blood Mononuclear Cells and Erythrocytes by Mycoplasma bovis

2010

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Mycoplasma bovis is a small, cell wall-less bacterium that contributes to a number of chronic inflammatory diseases in both dairy and feedlot cattle, including mastitis and bronchopneumonia. Numerous reports have implicated M. bovis in the activation of the immune system, while at the same time inhibiting immune cell proliferation. However, it is unknown whether the specific immune-cell population M. bovis is capable of attaching to and potentially invading. Here, we demonstrate that incubation of M. bovis Mb1 with bovine peripheral blood mononuclear cells (PBMC) resulted in a significant reduction in their proliferative responses while still remaining viable and capable of gamma interferon secretion. Furthermore, we show that M. bovis Mycoplasma bovis is a small, pleomorphic cell wall-less bacterium that is known to be a major contributing factor in the development of chronic pneumonia in feedlot cattle and mastitis in dairy cows. In addition to these two diseases, M. bovis has been linked to the development of otitis, keratoconjunctivitis, and arthritis (12). These diseases have large economic impacts, resulting in losses to both beef and dairy industries in Europe, Canada, and the United States (20). Furthermore, since M. bovis lacks a cell wall, the use of antibiotics to combat infections is limited, and the development of resistance to available antibiotics (tetracyclines and spectinomycin) has been observed (20). Interestingly, infection with M. bovis has been implicated in the potential exacerbation and enhancement of respiratory disease to other pathogens since coinfections with Histophilus somnus, bovine viral diarrhea virus, Mannheimia haemolytica, bovine respiratory syncytial virus, bovine parainfluenza virus type 3 have been observed (3,4,16,25). These findings suggest an important synergism in the development of disease during the coinfection of animals involving M. bovis and other pathogens.A number of factors appear to play an important role in the virulence and development of disease during M. bovis infection, although the specific mechanisms involved in these processes are still incompletely understood. M. bovis lacks a specialized organelle for attachment, as seen in M. pneumoniae and M. genitalium (1, 6), but instead expresses variable surface proteins (Vsps) that play a critical role in its attachment (24).These membrane surface proteins undergo substantial antigenic variation involving high-frequency phenotypic switching, resulting in an increased ability of M. bovis to evade the host's immune system (13,14,21). Furthermore, M. bovis can suppress the immune system via a secreted 26-amino-acid peptide that is 84% homologous to the C-terminal end of the VspL protein (33). This peptide appears to take part in the downregulation of lymphocyte proliferation and thereby ameliorates an appropriate immune response by the host. Another mechanism of immune evasion may involve the ability of M. bovis to inhibit neutrophil oxidative burst by a mechanism that appears to involve protein kinase C signaling...

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“…The intra-genic variations in the Mycoplasma bovis GAPDH gene were studied [52] and only small variations were observed. The antigenic conservation of the Mycoplasma bovis GAPDH suggests that this protein is a viable target for vaccine development.…”

Section: In Search Of a Vaccine For Mycoplasma Bovismentioning

confidence: 99%

GAPDH, as a Virulence Factor

Seidler

2012

GAPDH: Biological Properties and Diversity

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Pathogens, such as bacteria, viruses, protozoa and fungi, generate molecules that provide them with a selective advantage, often at the expense of the host. These molecules, or virulence factors, enable pathogens to colonize the host through several mechanisms. Some molecules offer the pathogen an advantage through better adhesion to host tissues, or superior invasive capability. Some allow the pathogen to evade or suppress the host's immune system. Some molecules enable intracellular parasites to disable cytoprotective mechansims, by re-directing the host phagocytic vesicles. Many of these molecules are proteins that are exported to the cell's surface or are secreted. As unlikely as it seems, GAPDH appears to play a role as a virulence factor in a number of pathogenic organisms by the mechanisms just described. This highly conserved protein is found on the outer surface or as a secretory product of these organisms. The process by which pathogenic GAPDH, which has >40 % sequence identity to human GAPDH, is exported and attached to the outer surface of cells remains unknown. This chapter also presents a previously unpublished proposed docking sequence on GAPDH. There is also discussion of the potential of using the antigenic properties of pathogenic GAPDH for medical as well as for veterinary purposes.

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Detection of antibodies against the Mycoplasma bovis glyceraldehyde-3-phosphate dehydrogenase protein in beef cattle

Cited by 41 publications

References 24 publications

In VitroInfection of Bovine Monocytes with Mycoplasma bovis Delays Apoptosis and Suppresses Production of Gamma Interferon and Tumor Necrosis Factor Alpha but Not Interleukin-10

In VitroInfection of Bovine Monocytes with Mycoplasma bovis Delays Apoptosis and Suppresses Production of Gamma Interferon and Tumor Necrosis Factor Alpha but Not Interleukin-10

Invasion of Bovine Peripheral Blood Mononuclear Cells and Erythrocytes by Mycoplasma bovis

GAPDH, as a Virulence Factor

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