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Пародонтоз может вызвать болезнь Альцгеймера.
Интерес исследователей вызвала бактерия Porphyromonas gingivalis. Она находится в полости рта, но может проникнуть в кровь и начать распространяться по организму, например, при повреждении десен зубной нитью.
Главная опасность этой бактерии заключается в синтезировании ферментов, которые разрушают связи между аминокислотами в белках. Антибиотики не могут ее уничтожить, а только вырабатывают устойчивость к лекарственным средствам.
Стефан Домини из американской компании Cortexyme, Ян Потемпа из Ягеллонского университета в Польше и их коллеги из других стран решили проверить, могут ли вырабатываемые этой бактерией ферменты провоцировать развитие болезни Альцгеймера.
Ученые изучили ткани мозга людей, страдавших болезнью Альцгеймера, и установили, что более 90% из 50 образцов содержали разные типы ферментов бактерии P. gingivalis.
Исследователям также удалось опытным путем установить взаимосвязь между появлением в клетках этих ферментов и повреждением тау-белков, которое и происходит в человеческом организме при болезни Альцгеймера.
Издание добавляет, что выводы ученых подтвердили результаты эксперимента, проведенного на мышах, которые также показали связь между заражением бактерией P. gingivalis и проявлениями болезни Альцгеймера. Об этом сообщает Рамблер. https://doctor.rambler.ru/pharma/416159 ... ntent=news


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СообщениеДобавлено: 30 янв 2019, 21:01 
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Сайт: http://www.dental-revue.ru
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Считают, что эта патогенная бактерия может нарушать иммунитет и способствовать появлению рака
Цитата:
J Oral Microbiol. 2019 Jan 9;11(1):1563410. doi: 10.1080/20002297.2018.1563410. eCollection 2019.

Possible role of Porphyromonas gingivalis in orodigestive cancers.

Olsen I1, Yilmaz Ö2.



Author information

1Department of Oral Biology, Faculty of Dentistry, University of Oslo, Oslo, Norway.2Department of Oral Health Sciences, Medical University of South Carolina, Charleston, SC, USA.
Abstract

There is increasing evidence for an association between periodontitis/tooth loss and oral, gastrointestinal, and pancreatic cancers. Periodontal disease, which is characterized by chronic inflammation and microbial dysbiosis, is a significant risk factor for orodigestive carcinogenesis. Porphyromonas gingivalis is proposed as a keystone pathogen in chronic periodontitis causing both dysbiosis and discordant immune response. The present review focuses on the growing recognition of a relationship between P. gingivalis and orodigestive cancers. Porphyromonas gingivalis has been recovered in abundance from oral squamous cell carcinoma (OSCC). Recently established tumorigenesis models have indicated a direct relationship between P. gingivalis and carcinogenesis. The bacterium upregulates specific receptors on OSCC cells and keratinocytes, induces epithelial-to-mesenchymal (EMT) transition of normal oral epithelial cells and activates metalloproteinase-9 and interleukin-8 in cultures of the carcinoma cells. In addition, P. gingivalis accelerates cell cycling and suppresses apoptosis in cultures of primary oral epithelial cells. In oral cancer cells, the cell cycle is arrested and there is no effect on apoptosis, but macro autophagy is increased. Porphyromonas gingivalis promotes distant metastasis and chemoresistance to anti-cancer agents and accelerates proliferation of oral tumor cells by affecting gene expression of defensins, by peptidyl-arginine deiminase and noncanonical activation of β-catenin. The pathogen also converts ethanol to the carcinogenic intermediate acetaldehyde. In addition, P. gingivalis can be implicated in precancerous gastric and colon lesions, esophageal squamous cell carcinoma, head and neck (larynx, throat, lip, mouth and salivary glands) carcinoma, and pancreatic cancer. The fact that distant organs can be involved clearly emphasizes that P. gingivalis has systemic tumorigenic effects in addition to the local effects in its native territory, the oral cavity. Although coinfection with other bacteria, viruses, and fungi occurs in periodontitis, P. gingivalis relates to cancer even in absence of periodontitis. Thus, there may be a direct relationship between P. gingivalis and orodigestive cancers.


Цитата:
Microorganisms. 2019 Jan 13;7(1). pii: E20. doi: 10.3390/microorganisms7010020.

Role of Oral Microbiota in Cancer Development.

Karpiński TM1.



Author information


Abstract

Nowadays cancer is the second main cause of death in the world. The most known bacterial carcinogen is Helicobacter pylori. Pathogens that can have an impact on cancer development in the gastrointestinal tract are also found in the oral cavity. Some specific species have been identified that correlate strongly with oral cancer, such as Streptococcus sp., Peptostreptococcus sp., Prevotella sp., Fusobacterium sp., Porphyromonas gingivalis, and Capnocytophaga gingivalis. Many works have also shown that the oral periopathogens Fusobacterium nucleatum and Porphyromonas gingivalis play an important role in the development of colorectal and pancreatic cancer. Three mechanisms of action have been suggested in regard to the role of oral microbiota in the pathogenesis of cancer. The first is bacterial stimulation of chronic inflammation. Inflammatory mediators produced in this process cause or facilitate cell proliferation, mutagenesis, oncogene activation, and angiogenesis. The second mechanism attributed to bacteria that may influence the pathogenesis of cancers by affecting cell proliferation is the activation of NF-κB and inhibition of cellular apoptosis. In the third mechanism, bacteria produce some substances that act in a carcinogenic manner. This review presents potentially oncogenic oral bacteria and possible mechanisms of their action on the carcinogenesis of human cells.

https://www.mdpi.com/2076-2607/7/1/20

Связь с болезнью Альцгеймера:
Цитата:
J Alzheimers Dis Rep. 2018 Dec 20;2(1):219-228. doi: 10.3233/ADR-180080.

Are Porphyromonas gingivalis Outer Membrane Vesicles Microbullets for Sporadic Alzheimer's Disease Manifestation?

Singhrao SK1, Olsen I2.



Author information


Abstract

Our research into Alzheimer's disease (AD) focuses on the oral cavity and the brain, from which key evaluations of prospective and retrospective population-based data have shown that chronic periodontal disease existing for ten-years or over doubles the risk for the sporadic form of AD. Furthermore, Porphyromonas gingivalis (P. gingivalis) mono-infections in established periodontal lesions, or introducing its lipopolysachharide (LPS), as demonstrated in in vivo studies, show hallmark pathology inclusive of extracellular amyloid plaques and phospho-tau bound neurofibrillary tangles with AD-like phenotype. Other studies have shown that if periodontitis remains untreated in human AD patients, cognitive decline ensues. This is a bi-directional relationship meaning that the converse is also true; treating periodontal disease in AD patients improves memory. Bacterial cultures and established oral biofilms generate vast numbers of microvesicles and P. gingivalis outer membrane vesicles encase key virulence factors (LPS, gingipains, capsule, fimbriae) as though they are complete destructive "microbullets" when shed in the host. This provides P. gingivalis additional arsenal to manipulate its entry into disparate organs, hijack phagocytosis, destroy tissues, and affect complement related genes while transducing the onset of proinflammatory signaling cascades. The resulting inflammatory mediators may be the cause of disease defining lesions and cognitive decline typical of clinical AD.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6311351/

Болезнь Альцгеймера, поражение коронарных сосудов сердца и диабет 2 типа:
Цитата:
Front Aging Neurosci. 2017 Dec 12;9:408. doi: 10.3389/fnagi.2017.00408. eCollection 2017.

The Porphyromonas gingivalis/Host Interactome Shows Enrichment in GWASdb Genes Related to Alzheimer's Disease, Diabetes and Cardiovascular Diseases.

Carter CJ1, France J2, Crean S2, Singhrao SK2.



Author information


Abstract

Periodontal disease is of established etiology in which polymicrobial synergistic ecology has become dysbiotic under the influence of Porphyromonas gingivalis. Following breakdown of the host's protective oral tissue barriers, P. gingivalis migrates to developing inflammatory pathologies that associate with Alzheimer's disease (AD). Periodontal disease is a risk factor for cardiovascular disorders (CVD), type II diabetes mellitus (T2DM), AD and other chronic diseases, whilst T2DM exacerbates periodontitis. This study analyzed the relationship between the P. gingivalis/host interactome and the genes identified in genome-wide association studies (GWAS) for the aforementioned conditions using data from GWASdb (P < 1E-03) and, in some cases, from the NCBI/EBI GWAS database (P < 1E-05). Gene expression data from periodontitis or P. gingivalis microarray was compared to microarray datasets from the AD hippocampus and/or from carotid artery plaques. The results demonstrated that the host genes of the P. gingivalis interactome were significantly enriched in genes deposited in GWASdb genes related to cognitive disorders, AD and dementia, and its co-morbid conditions T2DM, obesity, and CVD. The P. gingivalis/host interactome was also enriched in GWAS genes from the more stringent NCBI-EBI database for AD, atherosclerosis and T2DM. The misregulated genes in periodontitis tissue or P. gingivalis infected macrophages also matched those in the AD hippocampus or atherosclerotic plaques. Together, these data suggest important gene/environment interactions between P. gingivalis and susceptibility genes or gene expression changes in conditions where periodontal disease is a contributory factor.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5732932/


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