Pathogenic mechanisms of intracellular bacteria

Niller, Hans Helmut; Masa, Roland; Venkei, Annamária; Mészáros, Sándor; Minárovits, János

doi:10.1097/qco.0000000000000363

Cited by 25 publications

(17 citation statements)

References 77 publications

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“…M. hyorhinis encodes DNA-(cytosine-5)-methyltransferase enzymes that target CpG dinucleotides, establishing the methylation patterns of the bacterial genomes [57]. When expressed in human cells, they are able to translocate into the nucleus and create abnormal methylation patterns of the host cell DNA [57][58][59][60][61]. These epigenetics changes can contribute and lead to cancer progression by stimulating pro-oncogenic pathways.…”

Section: Mycoplasma and Cancermentioning

confidence: 99%

Role of Mycoplasma Chaperone DnaK in Cellular Transformation

Benedetti

Cocchi

Latinovic

et al. 2020

IJMS

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Studies of the human microbiome have elucidated an array of complex interactions between prokaryotes and their hosts. However, precise bacterial pathogen–cancer relationships remain largely elusive, although several bacteria, particularly those establishing persistent intra-cellular infections, like mycoplasmas, can alter host cell cycles, affect apoptotic pathways, and stimulate the production of inflammatory substances linked to DNA damage, thus potentially promoting abnormal cell growth and transformation. Consistent with this idea, in vivo experiments in several chemically induced or genetically deficient mouse models showed that germ-free conditions reduce colonic tumor formation. We demonstrate that mycoplasma DnaK, a chaperone protein belonging to the Heath shock protein (Hsp)-70 family, binds Poly-(ADP-ribose) Polymerase (PARP)-1, a protein that plays a critical role in the pathways involved in recognition of DNA damage and repair, and reduces its catalytic activity. It also binds USP10, a key p53 regulator, reducing p53 stability and anti-cancer functions. Finally, we showed that bystander, uninfected cells take up exogenous DnaK—suggesting a possible paracrine function in promoting cellular transformation, over and above direct mycoplasma infection. We propose that mycoplasmas, and perhaps certain other bacteria with closely related DnaK, may have oncogenic activity, mediated through the inhibition of DNA repair and p53 functions, and may be involved in the initiation of some cancers but not necessarily involved nor necessarily even be present in later stages.

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Section: Mycoplasma and Cancermentioning

confidence: 99%

Role of Mycoplasma Chaperone DnaK in Cellular Transformation

Benedetti

Cocchi

Latinovic

et al. 2020

IJMS

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show abstract

“…Also, there is marked hypomethylation of the IL8 promoter in oral epithelial cells of subjects with Generalized Aggressive Periodontitis compared to control subjects (Andia et al , 2010). Emerging studies suggest that microbial pathogens, including oral species such as Porphyromonas gingivalis, induce epigenetic modifications in host cells (reviewed in (Niller et al , 2017)). We recently identified potential epigenetic links between T. denticola and genes in PDL cells involved in activation of MMP-2 (Miao et al , 2014).…”

Section: Introductionmentioning

confidence: 99%

Treponema denticolaincreases MMP-2 expression and activation in the periodontium via reversible DNA and histone modifications

Ateia

Sutthiboonyapan

Kamarajan

et al. 2018

Cellular Microbiology

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Host-derived matrix metalloproteinases (MMPs) and bacterial proteases mediate destruction of extracellular matrices and supporting alveolar bone in periodontitis. The Treponema denticola dentilisin protease induces MMP-2 expression and activation in periodontal ligament (PDL) cells, and dentilisin-mediated activation of pro-MMP-2 is required for cellular fibronectin degradation. Here, we report that T. denticola regulates MMP-2 expression through epigenetic modifications in the periodontium. PDL cells were treated with epigenetic enzyme inhibitors before or after T. denticola challenge. Fibronectin fragmentation, MMP-2 expression, and activation were assessed by immunoblot, zymography, and qRT-PCR, respectively. Chromatin modification enzyme expression in T. denticola-challenged PDL cells and periodontal tissues were evaluated using gene arrays. Several classes of epigenetic enzymes showed significant alterations in transcription in diseased tissue and T. denticola-challenged PDL cells. T. denticola-mediated MMP-2 expression and activation were significantly reduced in PDL cells treated with inhibitors of aurora kinases and histone deacetylases. In contrast, DNA methyltransferase inhibitors had little effect, and inhibitors of histone acetyltransferases, methyltransferases, and demethylases exacerbated T. denticola-mediated MMP-2 expression and activation. Chronic epigenetic changes in periodontal tissues mediated by T. denticola or other oral microbes may contribute to the limited success of conventional treatment of chronic periodontitis and may be amenable to therapeutic reversal.

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“…Many intracellular bacteria are well-known pathogens, including Legionella pneumophila [ 51 ], Francissella tularensis [ 52 ], and Mycobacterium tuberculosis [ 53 ]. A. baumannii is also facultative intracellular bacteria [ 54 ], and had been reported to adhere and invade into human pulmonary cells, causing respiratory infections and pneumonia [ 55 – 57 ].…”

Section: Discussionmentioning

confidence: 99%

Postoperative infection caused by Acinetobacter baumannii misdiagnosed as a free-living amoeba species in a humeral head hemiarthroplasty patient: a case report

et al. 2018

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BackgroundAcinetobacter baumannii is ubiquitous, facultative intracellular, and opportunistic bacterial pathogen. Its unique abilities allow it to survive in a diverse range of environments, including health care settings, leading to nosocomial infections. And its exceptional ability to develop resistance to multiple antibiotics leaves few drug options for treatment. It has been recognized as a leading cause of nosocomial pneumonia and bacteremia over the world.Case presentationIn this case, a 73-year-old woman presented with a Neer Group VI proximal humeral fracture. Six hours after a successfully performed hemiarthroplasty, she developed continuous fever. Clinical examination revealed that the vitals were regular. Laboratory and radiographic examinations revealed only elevated procalcitonin levels. Blood culture revealed no bacterial or fungal growth. Cooling treatment and empirical broad-spectrum antibiotic therapy showed no apparent effect.ConclusionsWe report a postoperative infection caused by Acinetobacter baumannii. The infectious pathogen was identified via molecular DNA sequencing and was initially misidentified as a free-living amoeba species upon microscopic examinations. The patient was mistreated with antiamebic combination therapy. Her symptoms persisted for over 4 months and were eventually followed by her death.Electronic supplementary materialThe online version of this article (10.1186/s40249-018-0408-5) contains supplementary material, which is available to authorized users.

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Pathogenic mechanisms of intracellular bacteria

Abstract: Epigenetic regulators produced by intracellular bacteria alter the epigenotype and gene expression pattern of host cells and play an important role in pathogenesis.

Cited by 25 publications

References 77 publications

Role of Mycoplasma Chaperone DnaK in Cellular Transformation

Role of Mycoplasma Chaperone DnaK in Cellular Transformation

Treponema denticolaincreases MMP-2 expression and activation in the periodontium via reversible DNA and histone modifications

Postoperative infection caused by Acinetobacter baumannii misdiagnosed as a free-living amoeba species in a humeral head hemiarthroplasty patient: a case report

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