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Med Hypotheses ; 128: 25-27, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31203904


Nanobacteria or calcifying nanoparticles are 80-500 nm sized nano-organisms that are physically associated with carbonate apatite mineral formations. They have been indicated in various diseases, including kidney stone formation, Alzheimer's disease, and atherosclerosis. Nanoparticles contain calcium and apatite-binding protein fetuin-A, a calcification inhibitor. However, recent evidence indicates that fetuin-A can form nucleation seeds or nidi that grow in size through ion sedimentation to become larger amorphous nanoparticles in the presence of excess calcium and apatite ions. Fetuin-A also functions as an inhibitor of meprin, a metalloproteinase implicated in inflammation and neurodegenerative diseases. During inflammation, meprin functions to regulate chemokine activity of monocyte chemotactic protein 1, which is associated with chronic inflammatory diseases, including atherosclerosis, renal inflammatory diseases, and multiple sclerosis (MS). In addition, calcium phosphate nanocrystals that contain fetuin-A are pro-inflammatory to macrophages and promote vascular smooth muscle cell mineralization, potentiating a vicious cycle of inflammation and calcification. Thus, mineral stress and inflammation appear to be associated with each other. Furthermore, fetuin-A deficient mice exhibited reduced experimental autoimmune encephalomyelitis severity. Thus, fetuin-A plays a direct role in the neuroinflammatory response. Indeed, the level of fetuin-A in cerebrospinal fluid has been defined as a biomarker of disease activity in MS. MS is a chronic, inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS) with an unknown etiology. The "inside-out" model of MS, supported by recent data, states that the initial axonal degeneration in the CNS occurs before demyelination, which then stimulates an auto-immune attack. It was shown very recently that influx of calcium from the extracellular space through nanoscale ruptures of the axonal plasma membrane predict axon degeneration in neuroinflammation. Calcium is an activator of calpains, proteases that function to break down the cytoskeleton, leading to neurodegeneration. Nanoruptures of the plasma membrane were suggested to occur at the early stages of axon damage, especially at nodes of Ranvier, which are devoid of myelin. Here, I propose that calcifying nanoparticles may have a role in the etiology and/or pathophysiology of MS. The initial event causing neurodegeneration may be due to the nanoparticles that have been suggested to easily cross the blood-brain barrier. Following this, the nanoparticles may create nanoruptures in the axonal membrane and also increase the calcium concentration around and within the neurons by forming nidi for calcification, eventually causing neurodegeneration. Nanoparticles can self-replicate; hence, they may represent an infectious causative agent for the development of MS.

Nanopartículas Calcificantes/efeitos adversos , Calcinose/metabolismo , Esclerose Múltipla/etiologia , Animais , Apatitas/química , Barreira Hematoencefálica/metabolismo , Nanopartículas Calcificantes/química , Cálcio/química , Sistema Nervoso Central/metabolismo , Quimiocinas/metabolismo , Encefalomielite Autoimune Experimental/metabolismo , Humanos , Inflamação , Íons , Camundongos , Esclerose Múltipla/metabolismo , Doenças Neurodegenerativas/etiologia , Doenças Neurodegenerativas/metabolismo , alfa-2-Glicoproteína-HS/química
BMC Urol ; 17(1): 99, 2017 Oct 30.
Artigo em Inglês | MEDLINE | ID: mdl-29084530


BACKGROUND: Calcifying nanoparticles (NPs) have been proven to be associated with a variety of pathological calcification and previously detected in semen samples from patients with testicular microlithiasis (TM). The present study was designed to test the hypothesis if human-derived NPs could invade the seminiferous tubules and induce TM phenotype. METHODS: The animals were divided into three groups. Normal saline (0.2 mL) was injected into the proximal right ductus deferens in group A as a control group. The experimental groups, B and C received Escherichia coli (106 cfu/mL, 0.2 mL) and human-derived NPs suspension (0.2 mL), respectively. Rats were euthanized in 2 batches at 2 and 4 weeks. Testicular pathology, ultrastructure and inflammatory mediators were assessed. RESULTS: Chronic inflammatory changes were observed at 2 weeks in both groups B and C. Moreover, the innermost layer of sperm cells were structurally impaired and a zone of concentrically layered collagen fibers around the human NPs body was formed in the lumen of the seminiferous tubule in group C only, in which TM phenotype of remarkable calcification surrounded by cellular debris within the seminiferous tubules was built at 4 weeks. CONCLUSIONS: The results obtained from our study suggested a potential pathogenic effect of NPs in the development of calcification within the seminiferous tubules, which should be addressed in the future studies.

Nanopartículas Calcificantes/efeitos adversos , Cálculos/etiologia , Túbulos Seminíferos/patologia , Doenças Testiculares/etiologia , Animais , Calcinose/etiologia , Cálculos/patologia , Modelos Animais de Doenças , Escherichia coli , Humanos , Inflamação/etiologia , Masculino , Camundongos , Microscopia Eletrônica de Varredura , Ratos , Ratos Sprague-Dawley , Doenças Testiculares/patologia , Testículo/patologia , Testículo/ultraestrutura
Int J Nanomedicine ; 7: 339-50, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22287843


Calcifying nanoparticles (CNPs) (nanobacteria, nanobacteria-like particles, nanobes) were discovered over 25 years ago; nevertheless, their nature is still obscure. To date, nobody has been successful in credibly determining whether they are the smallest self-replicating life form on Earth, or whether they represent mineralo-protein complexes without any relation to living organisms. Proponents of both theories have a number of arguments in favor of the validity of their hypotheses. However, after epistemological analysis carried out in this review, all arguments used by proponents of the theory about the physicochemical model of CNP formation may be refuted on the basis of the performed investigations, and therefore published data suggest a biological nature of CNPs. The only obstacle to establish CNPs as living organisms is the absence of a fairly accurately sequenced genome at the present time. Moreover, it is clear that CNPs play an important role in etiopathogenesis of many diseases, and this association is independent from their nature. Consequently, emergence of CNPs in an organism is a pathological, not a physiological, process. The classification and new directions of further investigations devoted to the role of CNPs in biology and medicine are proposed.

Nanopartículas Calcificantes/efeitos adversos , Nanopartículas Calcificantes/isolamento & purificação , Calcinose/etiologia , Animais , Anticorpos/imunologia , Nanopartículas Calcificantes/análise , Nanopartículas Calcificantes/química , Nanopartículas Calcificantes/genética , Nanopartículas Calcificantes/imunologia , Nanopartículas Calcificantes/metabolismo , Calcinose/imunologia , Calcinose/microbiologia , Doença da Artéria Coronariana/microbiologia , Cistite/microbiologia , Humanos , Cálculos Renais/química , Cálculos Renais/microbiologia , Valva Mitral/microbiologia , Modelos Químicos