Hijacking of Host Plasminogen by
 Mesomycoplasma
 (
 Mycoplasma
 )
 hyopneumoniae
 via GAPDH: an Important Virulence Mechanism To Promote Adhesion and Extracellular Matrix Degradation

Wang, Jiying; Li, Shiyang; Chen, J; Gan, Lanxi; Wang, Jia; Xiong, Qiyan; Feng, Zhixin; Quan, Li; Deng, Zhibang; Yuan, Xianjun; Yu, Yafeng

doi:10.1128/spectrum.00218-23

Cited by 6 publications

(3 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Besides its primary role in translation, EF-Tu can also interact with host cells and contribute to the bacteria’s ability to adhere to and invade host tissues ( Yu et al., 2018 ). GAPDH has been implicated in adherence to host cells, invasion and modulation of the host immune response ( Wang et al., 2023a ). It can interact with host cell components and contribute to the bacteria’s ability to establish infection ( Wang et al., 2023b ).…”

Section: Resultsmentioning

confidence: 99%

The complete genome sequence of unculturable Mycoplasma faucium obtained through clinical metagenomic next-generation sequencing

Sabat,

Durfee,

Baldwin

et al. 2024

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

IntroductionDiagnosing Mycoplasma faucium poses challenges, and it's unclear if its rare isolation is due to infrequent occurrence or its fastidious nutritional requirements.MethodsThis study analyzes the complete genome sequence of M. faucium, obtained directly from the pus of a sternum infection in a lung transplant patient using metagenomic sequencing.ResultsGenome analysis revealed limited therapeutic options for the M. faucium infection, primarily susceptibility to tetracyclines. Three classes of mobile genetic elements were identified: two new insertion sequences, a new prophage (phiUMCG-1), and a species-specific variant of a mycoplasma integrative and conjugative element (MICE). Additionally, a Type I Restriction-Modification system was identified, featuring 5’-terminally truncated hsdS pseudogenes with overlapping repeats, indicating the potential for forming alternative hsdS variants through recombination.ConclusionThis study represents the first-ever acquisition of a complete circularized bacterial genome directly from a patient sample obtained from invasive infection of a primary sterile site using culture-independent, PCR-free clinical metagenomics.

show abstract

Section: Resultsmentioning

confidence: 99%

The complete genome sequence of unculturable Mycoplasma faucium obtained through clinical metagenomic next-generation sequencing

Sabat,

Durfee,

Baldwin

et al. 2024

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

show abstract

“…This allows the pathogen to evade removal by the host immune system and establish a persistent infection [80]. It is also possible that candidal GAPDH can affect the fibrinolysis cascade in a more general sense, e.g., by sequestering its soluble components via cell adsorption, resulting in pathway inhibition or, inversely, assembling the entire cascade on the pathogen surface, thereby enhancing fibrinolysis during infection [81]. The potential pathogenic role of HPG has been extensively studied in the context of its interactions with a major candidal moonlighting protein, enolase [50,66,82].…”

Section: Discussionmentioning

confidence: 99%

Glyceraldehyde 3-Phosphate Dehydrogenase on the Surface of Candida albicans and Nakaseomyces glabratus Cells—A Moonlighting Protein That Binds Human Vitronectin and Plasminogen and Can Adsorb to Pathogenic Fungal Cells via Major Adhesins Als3 and Epa6

Bednarek,

Satala,

Zawrotniak

et al. 2024

IJMS

View full text Add to dashboard Cite

Candida albicans and other closely related pathogenic yeast-like fungi carry on their surface numerous loosely adsorbed “moonlighting proteins”—proteins that play evolutionarily conserved intracellular functions but also appear on the cell surface and exhibit additional functions, e.g., contributing to attachment to host tissues. In the current work, we characterized this “moonlighting” role for glyceraldehyde 3-phosphate dehydrogenase (GAPDH, EC 1.2.1.12) of C. albicans and Nakaseomyces glabratus. GAPDH was directly visualized on the cell surface of both species and shown to play a significant part in the total capacity of fungal cells to bind two selected human host proteins—vitronectin and plasminogen. Using purified proteins, both host proteins were found to tightly interact with GAPDH, with dissociation constants in an order of 10−8 M, as determined by bio-layer interferometry and surface plasmon resonance measurements. It was also shown that exogenous GAPDH tightly adheres to the surface of candidal cells, suggesting that the cell surface location of this moonlighting protein may partly result from the readsorption of its soluble form, which may be present at an infection site (e.g., due to release from dying fungal cells). The major dedicated adhesins, covalently bound to the cell wall—agglutinin-like sequence protein 3 (Als3) and epithelial adhesin 6 (Epa6)—were suggested to serve as the docking platforms for GAPDH in C. albicans and N. glabratus, respectively.

show abstract

“…In the presence of a urokinase-type plasminogen activator (uPA), mycoplasma invasion becomes more pronounced (Yavlovich et al, 2001). In recent years, studies have shown that the protein or enzyme existing in mycoplasma itself can activate Plg and degrade ECM, such as Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) from M. hyopneumoniae (Wang et al, 2023). M. pneumoniae is not limited to the respiratory system but can invade vascular endothelial cells and lead to encephalitis (Rhodes et al, 2011).…”

Section: Distant Infectionmentioning

confidence: 99%

Unveiling the stealthy tactics: mycoplasma’s immune evasion strategies

Wang,

Liang,

Chen

et al. 2023

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

Mycoplasmas, the smallest known self-replicating organisms, possess a simple structure, lack a cell wall, and have limited metabolic pathways. They are responsible for causing acute or chronic infections in humans and animals, with a significant number of species exhibiting pathogenicity. Although the innate and adaptive immune responses can effectively combat this pathogen, mycoplasmas are capable of persisting in the host, indicating that the immune system fails to eliminate them completely. Recent studies have shed light on the intricate and sophisticated defense mechanisms developed by mycoplasmas during their long-term co-evolution with the host. These evasion strategies encompass various tactics, including invasion, biofilm formation, and modulation of immune responses, such as inhibition of immune cell activity, suppression of immune cell function, and resistance against immune molecules. Additionally, antigen variation and molecular mimicry are also crucial immune evasion strategies. This review comprehensively summarizes the evasion mechanisms employed by mycoplasmas, providing valuable insights into the pathogenesis of mycoplasma infections.

show abstract

Hijacking of Host Plasminogen by Mesomycoplasma ( Mycoplasma ) hyopneumoniae via GAPDH: an Important Virulence Mechanism To Promote Adhesion and Extracellular Matrix Degradation

Cited by 6 publications

References 43 publications

The complete genome sequence of unculturable Mycoplasma faucium obtained through clinical metagenomic next-generation sequencing

The complete genome sequence of unculturable Mycoplasma faucium obtained through clinical metagenomic next-generation sequencing

Glyceraldehyde 3-Phosphate Dehydrogenase on the Surface of Candida albicans and Nakaseomyces glabratus Cells—A Moonlighting Protein That Binds Human Vitronectin and Plasminogen and Can Adsorb to Pathogenic Fungal Cells via Major Adhesins Als3 and Epa6

Unveiling the stealthy tactics: mycoplasma’s immune evasion strategies

Contact Info

Product

Resources

About