Relationships Between Oral Microecosystem and Respiratory Diseases

Oral microecosystem is a very complicated ecosystem that is located in the mouth and comprises oral microbiome, diverse anatomic structures of oral cavity, saliva and interactions between oral microbiota and between oral microbiota and the host. More and more evidence from studies of epidemiology, microbiology and molecular biology is establishing a significant link between oral microecosystem and respiratory diseases. Microbiota settling down in oral microecosystem is known as the main source of lung microbiome and has been associated with the occurrence and development of respiratory diseases like pneumonia, chronic obstructive pulmonary disease, lung cancer, cystic fibrosis lung disease and asthma. In fact, it is not only indigenous oral microbes promote or directly cause respiratory infection and inflammation when inhaled into the lower respiratory tract, but also internal environment of oral microecosystem serves as a reservoir for opportunistic respiratory pathogens. Moreover, poor oral health and oral diseases caused by oral microecological dysbiosis (especially periodontal disease) are related with risk of multiple respiratory diseases. Here, we review the research status on the respiratory diseases related with oral microecosystem. Potential mechanisms on how respiratory pathogens colonize oral microecosystem and the role of indigenous oral microbes in pathogenesis of respiratory diseases are also summarized and analyzed. Given the importance of oral plaque control and oral health interventions in controlling or preventing respiratory infection and diseases, we also summarize the oral health management measures and attentions, not only for populations susceptible to respiratory infection like the elderly and hospitalized patients, but also for dentist or oral hygienists who undertake oral health care. In conclusion, the relationship between respiratory diseases and oral microecosystem has been established and supported by growing body of literature. However, etiological evidence on the role of oral microecosystem in the development of respiratory diseases is still insufficient. Further detailed studies focusing on specific mechanisms on how oral microecosystem participate in the pathogenesis of respiratory diseases could be helpful to prevent and treat respiratory diseases.

An Association of Pathogens and Biofilms with Alzheimer’s Disease

As one of the leading causes of dementia, Alzheimer’s disease (AD) is a condition in which individuals experience progressive cognitive decline. Although it is known that beta-amyloid (Aβ) deposits and neurofibrillary tangles (NFT) of tau fibrils are hallmark characteristics of AD, the exact causes of these pathologies are still mostly unknown. Evidence that infectious diseases may cause AD pathology has been accumulating for decades. The association between microbial pathogens and AD is widely studied, and there are noticeable correlations between some bacterial species and AD pathologies, especially spirochetes and some of the oral microbes. Borrelia burgdorferi has been seen to correlate with Aβ plaques and NFTs in infected cells. Because of the evidence of spirochetes in AD patients, Treponema pallidum and other oral treponemes are speculated to be a potential cause of AD. T. pallidum has been seen to form aggregates in the brain when the disease disseminates to the brain that closely resemble the Aβ plaques of AD patients. This review examines the evidence as to whether pathogens could be the cause of AD and its pathology. It offers novel speculations that treponemes may be able to induce or correlate with Alzheimer’s disease.

Assessment of Changes in the Oral Microbiome That Occur in Dogs with Periodontal Disease

The oral microbiome in dogs is a complex community. Under some circumstances, it contributes to periodontal disease, a prevalent inflammatory disease characterized by a complex interaction between oral microbes and the immune system. Porphyromonas and Tannerella spp. are usually dominant in this disease. How the oral microbiome community is altered in periodontal disease, especially sub-dominant microbial populations is unclear. Moreover, how microbiome functions are altered in this disease has not been studied. In this study, we compared the composition and the predicted functions of the microbiome of the cavity of healthy dogs to those with from periodontal disease. The microbiome of both groups clustered separately, indicating important differences. Periodontal disease resulted in a significant increase in Bacteroidetes and reductions in Actinobacteria and Proteobacteria. Porphyromonas abundance increased 2.7 times in periodontal disease, accompanied by increases in Bacteroides and Fusobacterium. It was predicted that aerobic respiratory processes are decreased in periodontal disease. Enrichment in fermentative processes and anaerobic glycolysis were suggestive of an anaerobic environment, also characterized by higher lipopolysaccharide biosynthesis. This study contributes to a better understanding of how periodontal disease modifies the oral microbiome and makes a prediction of the metabolic pathways that contribute to the inflammatory process observed in periodontal disease.

No evidence for colonization of oral bacteria in the distal gut in healthy adults

The microbial communities in the mouth and colon are anatomically connected via the saliva. However, the extent to which oral microbes reach and successfully colonize the distal gut has been debated. To resolve this long-standing controversy, we used exact amplicon sequence variants generated from concurrently collected saliva/stool microbiota in 66 healthy adults from two countries to show that, with one exception (Dialister invisus), the two niches are completely distinct. Thus, there is no evidence for colonization of oral bacteria in the distal gut. This defines the healthy state to which pathological states could be compared. Finding the same bacteria in the mouth and stool may warrant clinical investigation for an underlying pathology.

Looking For Polycyclic Aromatic Hydrocarbon Metabolizing Microorganisms In The Oral Cavity of Smokers

Certain soil microbes resist and metabolize polycyclic aromatic hydrocarbons (PAHs). The same is true for certain skin microbes. Oral microbes have the potential to oxidize tobacco PAHs to increase their ability to cause cancer. We hypothesized that oral microbes that resist high levels of PAH in smokers exist and can be identified based on their resistance to PAHs. We isolated bacteria and fungi that survived long term in minimal media with PAHs as the sole carbon source from the oral cavity in 11 of 14 smokers and only 1 of 6 nonsmokers. Of bacteria genera that included species that survived harsh PAH exposure in vitro, all were found at trace levels on the oral mucosa, except for Staphylococcus and Actinomyces. Two PAH-resistant strains of Candida albicans (C. albicans) were isolated from smokers. C. albicans is found orally at high levels in tobacco users and some Candida species can metabolize PAHs. The two C. albicans strains were tested for metabolism of two model PAH substrates, pyrene and phenanthrene. The result showed that the PAH-resistant C. albicans strains did not metabolize the two PAHs. In conclusion, evidence for large scale oral microbial metabolism of tobacco PAHs by common oral microbes remains lacking.

Correlation Between Salivary Microbiology and H2S Concentration of Oral Cavity

Background: Halitosis is caused by metabolites produced by oral microorganisms. Hydrogen sulfide is the most important compound that leads to the oral malodor, and is thought to be closely correlated with the activity of oral microorganism. Therefore, it is important to clarify the correlation between oral microbes and metabolites. Methods: Based on the 16S rRNA gene amplicon and shotgun metagenomic sequencing of oral microorganism, and oral malodor test, this study attempted to explain the contribution of oral microorganisms to the hydrogen sulfide of oral malodor. Results: The data shows that microbial taxa consisted in the H2S low and high groups are different, and most of the enriched taxa in the H2S high group are genus that correlated with H2S concentration. The two species Fusobaeterium periodonticum and Prevotella nanceiensis are significant different in both coverage breadth and depth and LPS biosynthesis contributions in two groups. According to KEGG metabolism pathways detected by HUMAnN2, subjects of the H2S high group may have a high risk to bacterial infection, since the LPS biosynthesis is enrichment. The contribution of F. periodonticum to sulfur metabolism between two groups is significantly different, and the relative abundance of F. periodonticum is higher in the H2S high group as well. Conclusions: The H2S content, is significantly associated with the composition and abundance of microorganisms in the oral cavity. The increase of microbial abundance and metabolism of some sulfide products are the main causes of halitosis. The most of the enriched microorganisms enriched in people with high H2S are associated with oral diseases such as caries and periodontal diseases, indicating that the diseases associated with oral microbes are not independent of each other and have some associations between some oral diseases.

Salivary bacterial signatures in depression-obesity comorbidity are associated with neurotransmitters and neuroactive dipeptides

BackgroundDepression and obesity, both of which are highly prevalent and inflammation underlies, often co-occur. Microbiome perturbations are implicated in obesity-inflammation-depression interrelationships, but how microbiome alterations contribute to underlying pathologic processes remains unclear. Metabolomic investigations to uncover microbial neuroactive metabolites may offer mechanistic insights into host-microbe interactions. MethodsUsing 16S sequencing and untargeted mass spectrometry of saliva, and blood monocyte inflammation regulation assays, we determined key microbes, metabolites and host inflammation in association with depressive symptomatology, obesity, and depressive symptomatology-obesity comorbidity. ResultsGram-negative bacteria with inflammation potential were enriched relative to Gram-positive bacteria in comorbid obesity-depression, supporting the inflammation-oral microbiome link in obesity-depression interrelationships. Oral microbiome was highly predictive of depressive symptomatology-obesity co-occurrences than obesity and depressive symptomatology independently, suggesting specific microbial signatures associated with obesity-depression co-occurrences. Mass spectrometry analysis revealed significant changes in levels of signaling molecules of microbiota, microbial or dietary derived signaling peptides and aromatic amino acids among host phenotypes. Furthermore, integration of the microbiome and metabolomics data revealed that key oral microbes, many previously shown to have neuroactive potential, co-occurred with potential neuropeptides and biosynthetic precursors of the neurotransmitters dopamine, epinephrine and serotonin. ConclusionsTogether, our findings offer novel insights into oral microbial-brain connection and potential neuroactive metabolites involved.

Salivary bacterial signatures in depression-obesity comorbidity are associated with neurotransmitters and neuroactive dipeptides

Depression and obesity, both of which are highly prevalent and inflammation underlies, often co-occur. Microbiome perturbations are implicated in obesity-inflammation-depression interrelationships, but how microbiome alterations contribute to underlying pathologic processes remains unclear. Metabolomic investigations to uncover microbial neuroactive metabolites may offer mechanistic insights into host-microbe interactions. Using 16S sequencing and untargeted mass spectrometry of saliva, and blood monocyte inflammation regulation assays, we determined key microbes, metabolites and host inflammation in association with depressive symptomatology, obesity, and depressive symptomatology-obesity comorbidity. Gram-negative bacteria with inflammation potential were enriched relative to Gram-positive bacteria in comorbid obesity-depression, supporting the inflammation-oral microbiome link in obesity-depression interrelationships. Oral microbiome was highly predictive of depressive symptomatology-obesity co-occurrences than obesity and depressive symptomatology independently, suggesting specific microbial signatures associated with obesity-depression co-occurrences. Mass spectrometry analysis revealed significant changes in levels of signaling molecules of microbiota, microbial or dietary derived signaling peptides and aromatic amino acids among host phenotypes. Furthermore, integration of the microbiome and metabolomics data revealed that key oral microbes, many previously shown to have neuroactive potential, co-occurred with potential neuropeptides and biosynthetic precursors of the neurotransmitters dopamine, epinephrine and serotonin. Together, our findings offer novel insights into oral microbial-brain connection and potential neuroactive metabolites involved.

Ethanol-Induced Cell Damage Can Result in the Development of Oral Tumors

Alcohol consumption is an underestimated risk factor for the development of precancerous lesions in the oral cavity. Although alcohol is a well-accepted recreational drug, 26.4% of all lip and oral cavity cancers worldwide are related to heavy drinking. Molecular mechanisms underlying this carcinogenic effect of ethanol are still under investigation. An important damaging effect comes from the first metabolite of ethanol, being acetaldehyde. Concentrations of acetaldehyde detected in the oral cavity are relatively high due to the metabolization of ethanol by oral microbes. Acetaldehyde can directly damage the DNA by the formation of mutagenic DNA adducts and interstrand crosslinks. Additionally, ethanol is known to affect epigenetic methylation and acetylation patterns, which are important regulators of gene expression. Ethanol-induced hypomethylation can activate the expression of oncogenes which subsequently can result in malignant transformation. The recent identification of ethanol-related mutational signatures emphasizes the role of acetaldehyde in alcohol-associated carcinogenesis. However, not all signatures associated with alcohol intake also relate to acetaldehyde. This finding highlights that there might be other effects of ethanol yet to be discovered.