Mycoplasma fermentans inhibits tumor necrosis factor α-induced apoptosis in the human myelomonocytic U937 cell line

Gerlic, Motti; Horowitz, J; Horowitz, Shulamith

doi:10.1038/sj.cdd.4401482

Cited by 21 publications

(18 citation statements)

References 36 publications

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“…U937 cells were grown in RPMI culture medium containing 10% fetal bovine serum (FBS), 1% penicillin-streptomycin and 1% 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid (HEPES), as described previously [39]. L929 and HaCaT cell TG macrophages were grown in DMEM culture medium containing 10% FBS, 1% penicillin-streptomycin, and 1% HEPES.…”

Section: Methodsmentioning

confidence: 99%

Phosphatidylserine externalization, “necroptotic bodies” release, and phagocytosis during necroptosis

et al. 2017

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Necroptosis is a regulated, nonapoptotic form of cell death initiated by receptor-interacting protein kinase-3 (RIPK3) and mixed lineage kinase domain-like (MLKL) proteins. It is considered to be a form of regulated necrosis, and, by lacking the “find me” and “eat me” signals that are a feature of apoptosis, necroptosis is considered to be inflammatory. One such “eat me” signal observed during apoptosis is the exposure of phosphatidylserine (PS) on the outer plasma membrane. Here, we demonstrate that necroptotic cells also expose PS after phosphorylated mixed lineage kinase-like (pMLKL) translocation to the membrane. Necroptotic cells that expose PS release extracellular vesicles containing proteins and pMLKL to their surroundings. Furthermore, inhibition of pMLKL after PS exposure can reverse the process of necroptosis and restore cell viability. Finally, externalization of PS by necroptotic cells drives recognition and phagocytosis, and this may limit the inflammatory response to this nonapoptotic form of cell death. The exposure of PS to the outer membrane and to extracellular vesicles is therefore a feature of necroptotic cell death and may serve to provide an immunologically-silent window by generating specific “find me” and “eat me” signals.

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Section: Methodsmentioning

confidence: 99%

Phosphatidylserine externalization, “necroptotic bodies” release, and phagocytosis during necroptosis

et al. 2017

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“…In addition, heat-inactivated M. fermentans was cytocidal for the human myelomonocytic cell line U937 by a mechanism that specifically excluded CD95 involvement (47). Infection with live M. fermentans did not induce apoptosis in U937 cells but, instead, protected against tumor necrosis factor alphainduced apoptosis through reduction of caspase-8 activity (25). M. alligatoris infection therefore is the first mycoplasmosis shown to influence an upstream element of the CD95 signal transduction pathway.…”

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confidence: 86%

Mycoplasma alligatorisInfection Promotes CD95 (FasR) Expression and Apoptosis of Primary Cardiac Fibroblasts

Hunt

Brown

2005

Clin Vaccine Immunol

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Mycoplasma alligatoris causes acute lethal primary infection of susceptible hosts. A genome survey implicated sialidase and hyaluronidase, potential promoters of CD95-mediated eukaryotic cell death, as virulence factors of M. alligatoris. We used immunofluorescence imaging and flow cytometry to examine the effects of M. alligatoris infection in vitro on CD95 expression and apoptosis by alligator cardiac fibroblasts, a major cell type of a target organ of M. alligatoris infection in vivo. A uniform distribution of CD95 in primary cultured cardiac, skeletal muscle, and embryonic fibroblasts was demonstrated by using polyclonal antibodies against the N or C terminus of mouse or human CD95. Anti-CD95 antibodies reacted on Western blots of fibroblast lysates with a band with the predicted apparent molecular weight of CD95, but soluble CD95 was not detected in plasma from control or M. alligatoris-infected alligators. The proportion of CD95-gated cardiac fibroblasts increased threefold (P < 0.01) 48 h after inoculation with M. alligatoris. Infection induced morphological changes in cardiac fibroblasts, including translocation of CD95 characteristic of apoptosis and an eightfold increase (P < 0.16) in 5-bromo-2-deoxyuridine (BrdU) incorporation measured in a terminal deoxynucleotide transferase dUTP nick end-labeling apoptosis assay. The proportion of BrdU-gated controls activated with agonistic immunoglobulin M against human CD95 also increased threefold (P < 0.03 for muscle). Heat-inactivated M. alligatoris and sterile M. alligatoris-conditioned culture supernatant had no effect. This is the first report of a CD95 homolog in the class Reptilia and establishes a new model that can be used to test the direct bacterial interaction with upstream components of the CD95 signal transduction pathway.In contrast to the usually subtle mycoplasmoses, Mycoplasma alligatoris causes acute lethal primary infection of susceptible hosts (7). Pathological changes in affected individuals reflect multisystem inflammatory disease, including necrotic epicarditis, pericarditis, and myocarditis (8, 9). A comparative genome survey approach to the identification of candidate virulence mechanisms revealed that M. alligatoris strain A21JP2 T possesses genes for the "spreading factors" sialidase (nanI) and hyaluronidase (nagH), a combination unprecedented among mycoplasmas (10). Functional studies demonstrated expression of the corresponding glycosidase activities, which might degrade host extracellular matrix (ECM) glycans to facilitate the rapid invasiveness of M. alligatoris infection (16,28,31,41,48). Its attenuated sibling species, Mycoplasma crocodyli strain MP145 T (43), also possesses hyaluronidase, so direct ECM damage alone seems insufficient to explain the particular virulence of M. alligatoris. M. crocodyli MP145 T does not possess sialidase (10). Desialylation of the eukaryotic cell death inducer CD95 (the fibroblast-associated receptor FasR) by sialidase substantially promoted CD95-mediated apoptosis in B-lineage leukemias and Jurk...

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“…Mycoplasma species are known for their apoptosis-modulating effects on host cells. However, these vary from apoptosis induction [25, 26] to inhibition of cell death [27, 28], indicating that additional research should be made to clarify these data.…”

Section: Discussionmentioning

confidence: 99%

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

Dušanić

Benčina

Narat

et al. 2014

BioMed Research International

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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.

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Mycoplasma fermentans inhibits tumor necrosis factor α-induced apoptosis in the human myelomonocytic U937 cell line

Cited by 21 publications

References 36 publications

Phosphatidylserine externalization, “necroptotic bodies” release, and phagocytosis during necroptosis

Phosphatidylserine externalization, “necroptotic bodies” release, and phagocytosis during necroptosis

Mycoplasma alligatorisInfection Promotes CD95 (FasR) Expression and Apoptosis of Primary Cardiac Fibroblasts

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

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