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1.
Front Cell Infect Microbiol ; 11: 706970, 2021.
Article in English | MEDLINE | ID: covidwho-1581382

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can cause gastrointestinal symptoms in the patients, but the role of gut microbiota in SARS-CoV-2 infection remains unclear. Thus, in this study, we aim to investigate whether SARS-CoV-2 infection affects the composition and function of gut microbiota. In this study, we demonstrated for the first time that significant shifts in microbiome composition and function were appeared in both SARS-CoV-2-infected asymptomatic and symptomatic cases. The relative abundance of Candidatus_Saccharibacteria was significantly increased, whereas the levels of Fibrobacteres was remarkably reduced in SARS-CoV-2-infected cases. There was one bacterial species, Spirochaetes displayed the difference between patients and asymptomatic cases. On the genus level, Tyzzerella was the key species that remarkably increased in both symptomatic and asymptomatic cases. Analyses of genome annotations further revealed SARS-CoV-2 infection resulted in the significant 'functional dysbiosis' of gut microbiota, including metabolic pathway, regulatory pathway and biosynthesis of secondary metabolites etc. We also identified potential metagenomic markers to discriminate SARS-CoV-2-infected symptomatic and asymptomatic cases from healthy controls. These findings together suggest gut microbiota is of possible etiological and diagnostic importance for SARS-CoV-2 infection.


Subject(s)
COVID-19 , Dysbiosis , Humans , Metagenome , Metagenomics , SARS-CoV-2
2.
Front Cell Infect Microbiol ; 10: 596166, 2020.
Article in English | MEDLINE | ID: covidwho-1574497

ABSTRACT

Viral infections continue to cause considerable morbidity and mortality around the world. Recent rises in these infections are likely due to complex and multifactorial external drivers, including climate change, the increased mobility of people and goods and rapid demographic change to name but a few. In parallel with these external factors, we are gaining a better understanding of the internal factors associated with viral immunity. Increasingly the gastrointestinal (GI) microbiome has been shown to be a significant player in the host immune system, acting as a key regulator of immunity and host defense mechanisms. An increasing body of evidence indicates that disruption of the homeostasis between the GI microbiome and the host immune system can adversely impact viral immunity. This review aims to shed light on our understanding of how host-microbiota interactions shape the immune system, including early life factors, antibiotic exposure, immunosenescence, diet and inflammatory diseases. We also discuss the evidence base for how host commensal organisms and microbiome therapeutics can impact the prevention and/or treatment of viral infections, such as viral gastroenteritis, viral hepatitis, human immunodeficiency virus (HIV), human papilloma virus (HPV), viral upper respiratory tract infections (URTI), influenza and SARS CoV-2. The interplay between the gastrointestinal microbiome, invasive viruses and host physiology is complex and yet to be fully characterized, but increasingly the evidence shows that the microbiome can have an impact on viral disease outcomes. While the current evidence base is informative, further well designed human clinical trials will be needed to fully understand the array of immunological mechanisms underlying this intricate relationship.


Subject(s)
Dysbiosis/virology , Microbiota/immunology , Probiotics/therapeutic use , Virus Diseases/immunology , Virus Diseases/microbiology , Animals , COVID-19/immunology , Dysbiosis/immunology , Gastrointestinal Microbiome/immunology , Host Microbial Interactions , Humans , SARS-CoV-2/isolation & purification , Viral Vaccines/administration & dosage , Viral Vaccines/immunology
3.
Rev Med Virol ; 31(5): 1-13, 2021 09.
Article in English | MEDLINE | ID: covidwho-1574011

ABSTRACT

Coronavirus disease 2019 (Covid-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, is now pandemic. While most Covid-19 patients will experience mild symptoms, a small proportion will develop severe disease, which could be fatal. Clinically, Covid-19 patients manifest fever with dry cough, fatigue and dyspnoea, and in severe cases develop into acute respiratory distress syndrome (ARDS), sepsis and multi-organ failure. These severe patients are characterized by hyperinflammation with highly increased pro-inflammatory cytokines including IL-6, IL-17 and TNF-alpha as well as C-reactive protein, which are accompanied by decreased lymphocyte counts. Clinical evidence supports that gut microbiota dysregulation is common in Covid-19 and plays a key role in the pathogenesis of Covid-19. In this narrative review, we summarize the roles of intestinal dysbiosis in Covid-19 pathogenesis and posit that the associated mechanisms are being mediated by gut bacterial metabolites. Based on this premise, we propose possible clinical implications. Various risk factors could be causal for severe Covid-19, and these include advanced age, concomitant chronic disease, SARS-CoV-2 infection of enterocytes, use of antibiotics and psychological distress. Gut dysbiosis is associated with risk factors and severe Covid-19 due to decreased commensal microbial metabolites, which cause reduced anti-inflammatory mechanisms and chronic low-grade inflammation. The preconditioned immune dysregulation enables SARS-CoV-2 infection to progress to an uncontrolled hyperinflammatory response. Thus, a pre-existing gut microbiota that is diverse and abundant could be beneficial for the prevention of severe Covid-19, and supplementation with commensal microbial metabolites may facilitate and augment the treatment of severe Covid-19.


Subject(s)
Bacteria/metabolism , COVID-19/microbiology , Gastrointestinal Microbiome , Animals , Bacteria/classification , Bacteria/genetics , Bacteria/isolation & purification , COVID-19/genetics , COVID-19/immunology , COVID-19/virology , Cytokines/genetics , Cytokines/immunology , Dysbiosis/genetics , Dysbiosis/immunology , Dysbiosis/microbiology , Dysbiosis/virology , Humans , SARS-CoV-2/genetics , SARS-CoV-2/physiology
4.
Cells ; 10(12)2021 11 25.
Article in English | MEDLINE | ID: covidwho-1542428

ABSTRACT

Acute respiratory distress syndrome (ARDS) is a serious lung condition characterized by severe hypoxemia leading to limitations of oxygen needed for lung function. In this study, we investigated the effect of anandamide (AEA), an endogenous cannabinoid, on Staphylococcal enterotoxin B (SEB)-mediated ARDS in female mice. Single-cell RNA sequencing data showed that the lung epithelial cells from AEA-treated mice showed increased levels of antimicrobial peptides (AMPs) and tight junction proteins. MiSeq sequencing data on 16S RNA and LEfSe analysis demonstrated that SEB caused significant alterations in the microbiota, with increases in pathogenic bacteria in both the lungs and the gut, while treatment with AEA reversed this effect and induced beneficial bacteria. AEA treatment suppressed inflammation both in the lungs as well as gut-associated mesenteric lymph nodes (MLNs). AEA triggered several bacterial species that produced increased levels of short-chain fatty acids (SCFAs), including butyrate. Furthermore, administration of butyrate alone could attenuate SEB-mediated ARDS. Taken together, our data indicate that AEA treatment attenuates SEB-mediated ARDS by suppressing inflammation and preventing dysbiosis, both in the lungs and the gut, through the induction of AMPs, tight junction proteins, and SCFAs that stabilize the gut-lung microbial axis driving immune homeostasis.


Subject(s)
Arachidonic Acids/therapeutic use , Endocannabinoids/therapeutic use , Gastrointestinal Microbiome , Gastrointestinal Tract/pathology , Lung/pathology , Polyunsaturated Alkamides/therapeutic use , Respiratory Distress Syndrome/drug therapy , Respiratory Distress Syndrome/microbiology , Animals , Arachidonic Acids/pharmacology , Butyrates/metabolism , Cecum/pathology , Cell Separation , Colon/drug effects , Colon/pathology , Discriminant Analysis , Dysbiosis/complications , Dysbiosis/microbiology , Endocannabinoids/pharmacology , Enterotoxins , Female , Gastrointestinal Tract/drug effects , Lymph Nodes/drug effects , Lymph Nodes/pathology , Lymphocyte Activation/drug effects , Mice, Inbred C57BL , Pneumonia/drug therapy , Pneumonia/microbiology , Polyunsaturated Alkamides/pharmacology , Respiratory Distress Syndrome/complications , T-Lymphocytes/drug effects
5.
Biomed J ; 44(4): 504-507, 2021 08.
Article in English | MEDLINE | ID: covidwho-1525701

ABSTRACT

COVID-19, an infectious disease caused by a novel coronavirus (SARS-CoV-2) has emerged as global pandemic. Here, we described the changes in microbiota of upper respiratory tract by analyzing the publically available RNA sequencing data of SARS-CoV-2-infected ferrets. The bacterial dysbiosis due to SARS-CoV-2 was largely inversely proportional to the dysbiosis caused by influenza-A virus. The bacterial taxa which are defined as healthy ecostate were significantly reduced during SARS-CoV-2 infection. Altogether, this preliminary study provides a new insight on the possible role of bacterial communities of upper respiratory tract in determining the immunity, susceptibility, and mortality for COVID-19.


Subject(s)
COVID-19 , Microbiota , Animals , Dysbiosis , Ferrets , Humans , Microbiota/genetics , RNA , Respiratory System , SARS-CoV-2 , Sequence Analysis, RNA
6.
Front Immunol ; 12: 765965, 2021.
Article in English | MEDLINE | ID: covidwho-1497082

ABSTRACT

Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), resulted in an unprecedented global crisis. Although primarily a respiratory illness, dysregulated immune responses may lead to multi-organ dysfunction. Prior data showed that the resident microbial communities of gastrointestinal and respiratory tracts act as modulators of local and systemic inflammatory activity (the gut-lung axis). Evolving evidence now signals an alteration in the gut microbiome, brought upon either by cytokines from the infected respiratory tract or from direct infection of the gut, or both. Dysbiosis leads to a "leaky gut". The intestinal permeability then allows access to bacterial products and toxins into the circulatory system and further exacerbates the systemic inflammatory response. In this review, we discuss the available data related to the role of the gut microbiome in the development and progression of COVID-19. We provide mechanistic insights into early data with a focus on immunological crosstalk and the microbiome's potential as a biomarker and therapeutic target.


Subject(s)
COVID-19/microbiology , Cytokine Release Syndrome/microbiology , Dysbiosis/microbiology , Gastrointestinal Microbiome/immunology , SARS-CoV-2/physiology , COVID-19/immunology , Cytokine Release Syndrome/immunology , Dysbiosis/immunology , Humans , Immunity , Inflammation
7.
Sci Rep ; 11(1): 21297, 2021 10 29.
Article in English | MEDLINE | ID: covidwho-1493220

ABSTRACT

The COVID-19 outbreak has caused over three million deaths worldwide. Understanding the pathology of the disease and the factors that drive severe and fatal clinical outcomes is of special relevance. Studying the role of the respiratory microbiota in COVID-19 is especially important as the respiratory microbiota is known to interact with the host immune system, contributing to clinical outcomes in chronic and acute respiratory diseases. Here, we characterized the microbiota in the respiratory tract of patients with mild, severe, or fatal COVID-19, and compared it to healthy controls and patients with non-COVID-19-pneumonia. We comparatively studied the microbial composition, diversity, and microbiota structure between the study groups and correlated the results with clinical data. We found differences in the microbial composition for COVID-19 patients, healthy controls, and non-COVID-19 pneumonia controls. In particular, we detected a high number of potentially opportunistic pathogens associated with severe and fatal levels of the disease. Also, we found higher levels of dysbiosis in the respiratory microbiota of patients with COVID-19 compared to the healthy controls. In addition, we detected differences in diversity structure between the microbiota of patients with mild, severe, and fatal COVID-19, as well as the presence of specific bacteria that correlated with clinical variables associated with increased risk of mortality. In summary, our results demonstrate that increased dysbiosis of the respiratory tract microbiota in patients with COVID-19 along with a continuous loss of microbial complexity structure found in mild to fatal COVID-19 cases may potentially alter clinical outcomes in patients. Taken together, our findings identify the respiratory microbiota as a factor potentially associated with the severity of COVID-19.


Subject(s)
Bacteria/genetics , COVID-19/microbiology , COVID-19/mortality , Dysbiosis/microbiology , Microbiota/genetics , Respiratory System/microbiology , SARS-CoV-2/genetics , Severity of Illness Index , Adolescent , Adult , Aged , COVID-19/pathology , Case-Control Studies , Female , Humans , Kaplan-Meier Estimate , Male , Middle Aged , Phylogeny , RNA, Ribosomal, 16S/genetics , Young Adult
8.
Expert Rev Gastroenterol Hepatol ; 15(11): 1281-1294, 2021 Nov.
Article in English | MEDLINE | ID: covidwho-1470080

ABSTRACT

INTRODUCTION: Human gut microbiota plays a crucial role in providing protective responses against pathogens, particularly by regulating immune system homeostasis. There is a reciprocal interaction between the gut and lung microbiota, called the gut-lung axis (GLA). Any alteration in the gut microbiota or their metabolites can cause immune dysregulation, which can impair the antiviral activity of the immune system against respiratory viruses such as severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV-2. AREAS COVERED: This narrative review mainly outlines emerging data on the mechanisms underlying the interactions between the immune system and intestinal microbial dysbiosis, which is caused by an imbalance in the levels of essential metabolites. The authors will also discuss the role of probiotics in restoring the balance of the gut microbiota and modulation of cytokine storm. EXPERT OPINION: Microbiota-derived signals regulate the immune system and protect different tissues during severe viral respiratory infections. The GLA's equilibration could help manage the mortality and morbidity rates associated with SARS-CoV-2 infection.


Subject(s)
COVID-19/immunology , Dysbiosis/immunology , Gastrointestinal Microbiome/immunology , Immune System/immunology , Pneumonia, Viral/immunology , Humans , SARS-CoV-2
9.
Microbiol Spectr ; 9(2): e0005521, 2021 10 31.
Article in English | MEDLINE | ID: covidwho-1467670

ABSTRACT

Bacterial-viral interactions in saliva have been associated with morbidity and mortality for respiratory viruses such as influenza and SARS-CoV. However, such transkingdom relationships during SARS-CoV-2 infection are currently unknown. Here, we aimed to elucidate the relationship between saliva microbiota and SARS-CoV-2 in a cohort of newly hospitalized COVID-19 patients and controls. We used 16S rRNA sequencing to compare microbiome diversity and taxonomic composition between COVID-19 patients (n = 53) and controls (n = 59) and based on saliva SARS-CoV-2 viral load as measured using reverse transcription PCR (RT-PCR). The saliva microbiome did not differ markedly between COVID-19 patients and controls. However, we identified significant differential abundance of numerous taxa based on saliva SARS-CoV-2 viral load, including multiple species within Streptococcus and Prevotella. IMPORTANCE Alterations to the saliva microbiome based on SARS-CoV-2 viral load indicate potential biologically relevant bacterial-viral relationships which may affect clinical outcomes in COVID-19 disease.


Subject(s)
Bacteria/classification , COVID-19/pathology , Microbial Interactions/physiology , SARS-CoV-2/isolation & purification , Saliva/microbiology , Bacteria/genetics , Dysbiosis/microbiology , Female , Humans , Male , Microbiota/genetics , Middle Aged , Nasopharynx/microbiology , RNA, Ribosomal, 16S/genetics , Viral Load
10.
Gut Microbes ; 13(1): 1984105, 2021.
Article in English | MEDLINE | ID: covidwho-1462225

ABSTRACT

Infection with severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) is responsible for the COVID-19 pandemic. Angiotensin-converting enzyme 2 (Ace2) is expressed in the gastrointestinal (GI) tract and a receptor for SARS-CoV-2, making the GI tract a potential infection site. This study investigated the effects of commensal intestinal microbiota on colonic Ace2 expression using a humanized mouse model. We found that colonic Ace2 expression decreased significantly upon microbial colonization. Humanization with healthy volunteer or dysbiotic microbiota from irritable bowel syndrome (IBS) patients resulted in similar Ace2 expression. Despite the differences in microbiota, no associations between α-diversity, ß-diversity or individual taxa, and Ace2 were noted post-humanization. These results highlight that commensal microbiota play a key role in regulating intestinal Ace2 expression and the need to further examine the underlying mechanisms of this regulation.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , Colon/metabolism , Gastrointestinal Microbiome , Animals , Colon/microbiology , Dysbiosis , Gene Expression Regulation , Germ-Free Life , Humans , Inflammatory Bowel Diseases/microbiology , Mice , Receptors, Virus/metabolism , SARS-CoV-2
11.
BMC Microbiol ; 21(1): 277, 2021 10 11.
Article in English | MEDLINE | ID: covidwho-1463230

ABSTRACT

BACKGROUND: Fusobacterium nucleatum (F. n) is an important opportunistic pathogen causing oral and gastrointestinal disease. Faecalibacterium prausnitzii (F. p) is a next-generation probiotic and could serve as a biomarker of gut eubiosis/dysbiosis to some extent. Alterations in the human oral and gut microbiomes are associated with viral respiratory infection. The aim of this study was to characterise the oral and fecal bacterial biomarker (i.e., F. n and F. p) in COVID-19 patients by qPCR and investigate the pharyngeal microbiome of COVID-19 patients through metagenomic next-generation sequencing (mNGS). RESULTS: Pharyngeal F. n was significantly increased in COVID-19 patients, and it was higher in male than female patients. Increased abundance of pharyngeal F. n was associated with a higher risk of a positive SARS-CoV-2 test (adjusted OR = 1.32, 95% CI = 1.06 ~ 1.65, P < 0.05). A classifier to distinguish COVID-19 patients from the healthy controls based on the pharyngeal F. n was constructed and achieved an area under the curve (AUC) of 0.843 (95% CI = 0.688 ~ 0.940, P < 0.001). However, the level of fecal F. n and fecal F. p remained unaltered between groups. Besides, mNGS showed that the pharyngeal swabs of COVID-19 patients were dominated by opportunistic pathogens. CONCLUSIONS: Pharyngeal but not fecal F. n was significantly increased in COVID-19 patients, clinicians should pay careful attention to potential coinfection. Pharyngeal F. n may serve as a promising candidate indicator for COVID-19.


Subject(s)
COVID-19/microbiology , Feces/microbiology , Fusobacterium Infections/microbiology , Fusobacterium nucleatum/genetics , Pharynx/microbiology , Adult , Biomarkers/analysis , COVID-19/virology , Carrier State/microbiology , Coinfection/microbiology , Coinfection/virology , Dysbiosis , Female , Fusobacterium Infections/virology , High-Throughput Nucleotide Sequencing , Humans , Male , Metagenomics , Microbiota , Middle Aged , Pharynx/virology , Sex Factors
12.
Biomed Res Int ; 2021: 7880448, 2021.
Article in English | MEDLINE | ID: covidwho-1455779

ABSTRACT

COVID-19-associated neuropsychiatric complications are soaring. There is an urgent need to understand the link between COVID-19 and neuropsychiatric disorders. To that end, this article addresses the premise that SARS-CoV-2 infection results in gut dysbiosis and an altered microbiota-gut-brain (MGB) axis that in turn contributes to the neuropsychiatric ramifications of COVID-19. Altered MGB axis activity has been implicated independently as a risk of neuropsychiatric disorders. A review of the changes in gut microbiota composition in individual psychiatric and neurological disorders and gut microbiota in COVID-19 patients revealed a shared "microbial signature" characterized by a lower microbial diversity and richness and a decrease in health-promoting anti-inflammatory commensal bacteria accompanied by an increase in opportunistic proinflammatory pathogens. Notably, there was a decrease in short-chain fatty acid (SCFA) producing bacteria. SCFAs are key bioactive microbial metabolites with anti-inflammatory functions and have been recognized as a critical signaling pathway in the MGB axis. SCFA deficiency is associated with brain inflammation, considered a cardinal feature of neuropsychiatric disorders. The link between SARS-CoV-2 infection, gut dysbiosis, and altered MGB axis is further supported by COVID-19-associated gastrointestinal symptoms, a high number of SARS-CoV-2 receptors, angiotensin-cleaving enzyme-2 (ACE-2) in the gut, and viral presence in the fecal matter. The binding of SARS-CoV-2 to the receptor results in ACE-2 deficiency that leads to decreased transport of vital dietary components, gut dysbiosis, proinflammatory gut status, increased permeability of the gut-blood barrier (GBB), and systemic inflammation. More clinical research is needed to substantiate further the linkages described above and evaluate the potential significance of gut microbiota as a diagnostic tool. Meanwhile, it is prudent to propose changes in dietary recommendations in favor of a high fiber diet or supplementation with SCFAs or probiotics to prevent or alleviate the neuropsychiatric ramifications of COVID-19.


Subject(s)
COVID-19/psychology , Fatty Acids, Volatile/metabolism , Gastrointestinal Microbiome/physiology , Bacteria/metabolism , Brain/metabolism , Brain/pathology , COVID-19/metabolism , COVID-19/microbiology , COVID-19/virology , Diet , Dysbiosis , Feces/microbiology , Gastrointestinal Diseases/microbiology , Gastrointestinal Microbiome/immunology , Humans , Inflammation , Probiotics/pharmacology , SARS-CoV-2/isolation & purification
13.
Nutrients ; 13(9)2021 Aug 24.
Article in English | MEDLINE | ID: covidwho-1448913

ABSTRACT

The human body is host to a large number of microorganisms which conform the human microbiota, that is known to play an important role in health and disease. Although most of the microorganisms that coexist with us are located in the gut, microbial cells present in other locations (like skin, respiratory tract, genitourinary tract, and the vaginal zone in women) also play a significant role regulating host health. The fact that there are different kinds of microbiota in different body areas does not mean they are independent. It is plausible that connection exist, and different studies have shown that the microbiota present in different zones of the human body has the capability of communicating through secondary metabolites. In this sense, dysbiosis in one body compartment may negatively affect distal areas and contribute to the development of diseases. Accordingly, it could be hypothesized that the whole set of microbial cells that inhabit the human body form a system, and the dialogue between the different host microbiotas may be a contributing factor for the susceptibility to developing diseased states. For this reason, the present review aims to integrate the available literature on the relationship between the different human microbiotas and understand how changes in the microbiota in one body region can influence other microbiota communities in a bidirectional process. The findings suggest that the different microbiotas may act in a coordinated way to decisively influence human well-being. This new integrative paradigm opens new insights in the microbiota field of research and its relationship with human health that should be taken into account in future studies.


Subject(s)
Dysbiosis/metabolism , Microbiota , Female , Gastrointestinal Microbiome , Health Status , Humans , Male , Mouth/microbiology , Respiratory System/microbiology , Skin/microbiology , Urogenital System/microbiology , Vagina/microbiology
14.
Nutrients ; 13(8)2021 Jul 27.
Article in English | MEDLINE | ID: covidwho-1430928

ABSTRACT

Gut microbiota has emerged as a major metabolically active organ with critical functions in both health and disease. The trillions of microorganisms hosted by the gastrointestinal tract are involved in numerous physiological and metabolic processes including modulation of appetite and regulation of energy in the host spanning from periphery to the brain. Indeed, bacteria and their metabolic byproducts are working in concert with the host chemosensory signaling pathways to affect both short- and long-term ingestive behavior. Sensing of nutrients and taste by specialized G protein-coupled receptor cells is important in transmitting food-related signals, optimizing nutrition as well as in prevention and treatment of several diseases, notably obesity, diabetes and associated metabolic disorders. Further, bacteria metabolites interact with specialized receptors cells expressed by gut epithelium leading to taste and appetite response changes to nutrients. This review describes recent advances on the role of gut bacteria in taste perception and functions. It further discusses how intestinal dysbiosis characteristic of several pathological conditions may alter and modulate taste preference and food consumption via changes in taste receptor expression.


Subject(s)
Bacterial Physiological Phenomena , Gastrointestinal Microbiome/physiology , Intestines/microbiology , Taste Perception , Animals , Antineoplastic Agents/therapeutic use , Bariatric Surgery , COVID-19/physiopathology , Diet , Dysbiosis/physiopathology , Feeding Behavior , Hormones/metabolism , Humans , Inflammatory Bowel Diseases/physiopathology , Neoplasms/drug therapy , Neoplasms/physiopathology , Receptors, G-Protein-Coupled/metabolism , Taste , Taste Buds/physiology , Toll-Like Receptors/metabolism
15.
Periodontol 2000 ; 87(1): 94-106, 2021 10.
Article in English | MEDLINE | ID: covidwho-1383455

ABSTRACT

Chronic stress is a relevant disease to periodontal practice, encompassing 25%-28% of the US population (American Psychological Association 2015). While it is well established that chronic psychologic stress can have significant deleterious systemic effects, only in recent decades have we begun to explore the biochemical, microbial, and physiologic impacts of chronic stress diseases on oral tissues. Currently, chronic stress is classified as a "risk indicator" for periodontal disease. However, as the evidence in this field matures with additional clinically controlled trials, more homogeneous data collection methods, and a better grasp of the biologic underpinnings of stress-mediated dysbiosis, emerging evidence suggests that chronic stress and related diseases (depression, anxiety) may be significant contributing factors in periodontal/peri-implant disease progression and inconsistent wound healing following periodontal-related therapeutics. Ideal solutions for these patients include classification of the disease process and de-escalation of chronic stress conditions through coping strategies. This paper also summarizes periodontal/implant-related therapeutic approaches to ensure predictable results for this specific patient subpopulation.


Subject(s)
Dental Implants , Peri-Implantitis , Periodontal Diseases , Dysbiosis , Humans , Periodontal Diseases/therapy , Wound Healing
16.
Periodontol 2000 ; 87(1): 11-16, 2021 10.
Article in English | MEDLINE | ID: covidwho-1379599

ABSTRACT

The landscape in dentistry is changing as emerging studies continue to reveal that periodontal health impacts systemic health, and vice versa. Population studies, clinical studies, and in vitro animal studies underscore the critical importance of oral health to systemic health. These inextricable relationships come to the forefront as oral diseases, such as periodontal disease, take root. Special populations bring to bear the multimodal relationships between oral and systemic health. Specifically, periodontal disease has been associated with diabetes, metabolic syndrome, obesity, eating disorders, liver disease, cardiovascular disease, Alzheimer disease, rheumatoid arthritis, adverse pregnancy outcomes, and cancer. Although bidirectional relationships are recognized, the potential for multiple comorbidities, relationships, and connections (multimodal relationships) also exists. Proposed mechanisms that mediate this connection between oral and systemic health include predisposing and precipitating factors, such as genetic factors (gene polymorphisms), environmental factors (stress, habits-such as smoking and high-fat diets/consumption of highly processed foods), medications, microbial dysbiosis and bacteremias/viremias/microbemias, and an altered host immune response. Thus, in a susceptible host, these predisposing and precipitating factors trigger the onset of periodontal disease and systemic disease/conditions. Further, high-throughput sequencing technologies are shedding light on the dark matter that comprises the oral microbiome. This has resulted in better characterization of the oral microbial dysbiosis, including putative bacterial periodontopathogens and shifts in oral virome composition during disease. Multiple laboratory and clinical studies have illustrated that both eukaryotic and prokaryotic viruses within subgingival plaque and periodontal tissues affect periodontal inflammation, putative periodontopathogens, and the host immune response. Although the association between herpesviruses and periodontitis and the degree to which these viruses directly aggravate periodontal tissue damage remain unclear, the benefits to periodontal health found from prolonged administration of antivirals in immunocompromised or immunodeficient individuals demonstrates that specific populations are possibly more susceptible to viral periodontopathogens. Thus, it may be important to further examine the implications of viral pathogen involvement in periodontitis and perhaps it is time to embrace the viral dark matter within the periodontal environment to fully comprehend the pathogenesis and systemic implications of periodontitis. Emerging data from the coronavirus disease 2019 pandemic further underscores the inextricable connection between oral and systemic health, with high levels of the severe acute respiratory syndrome coronavirus 2 angiotensin-converting enzyme 2 receptor noted on oral tissues (tongue) and an allostatic load or overload paradigm of chronic stress likely contributing to rapid breakdown of oral/dental, periodontal, and peri-implant tissues. These associations exist within a framework of viremias/bacteremias/microbemias, systemic inflammation, and/or disturbances of the immune system in a susceptible host. A thorough review of systemic and oral diseases and conditions and their mechanistic, predisposing, and precipitating factors are paramount to better addressing the oral and systemic health and needs of our patients.


Subject(s)
COVID-19 , Periodontal Diseases , Animals , Dysbiosis , Female , Humans , Oral Health , Pregnancy , SARS-CoV-2
17.
J Immunotoxicol ; 18(1): 93-104, 2021 07 24.
Article in English | MEDLINE | ID: covidwho-1373514

ABSTRACT

The aging immune system is characterized by a low-grade chronic systemic inflammatory state ("inflammaging") marked by elevated serum levels of inflammatory molecules such as interleukin (IL)-6 and C-reactive protein (CRP). These inflammatory markers were also reported to be strong predictors for the development/severity of Type 2 diabetes, obesity, and COVID-19. The levels of these markers have been positively associated with those of advanced glycation end-products (AGEs) generated via non-enzymatic glycation and oxidation of proteins and lipids during normal aging and metabolism. Based on the above observations, it is clinically important to elucidate how dietary AGEs modulate inflammation and might thus increase the risk for aging-exacerbated diseases. The present narrative review discusses the potential pro-inflammatory properties of dietary AGEs with a focus on the inflammatory mediators CRP, IL-6 and ferritin, and their relations to aging in general and Type 2 diabetes in particular. In addition, underlying mechanisms - including those related to gut microbiota and the receptors for AGEs, and the roles AGEs might play in affecting physiologies of the healthy elderly, obese individuals, and diabetics are discussed in regard to any greater susceptibility to COVID-19.


Subject(s)
COVID-19/metabolism , Diabetes Mellitus, Type 2/metabolism , Glycation End Products, Advanced/metabolism , Inflammation Mediators/metabolism , SARS-CoV-2/physiology , Aging , Animals , Diet , Dysbiosis , Gastrointestinal Microbiome , Glycation End Products, Advanced/immunology , Homeostasis , Humans , Immunity , Lipid Metabolism
18.
Cells ; 10(6)2021 06 17.
Article in English | MEDLINE | ID: covidwho-1369745

ABSTRACT

Hypertension is associated with gut bacterial dysbiosis and gut pathology in animal models and people. Butyrate-producing gut bacteria are decreased in hypertension. RNA-seq analysis of gut colonic organoids prepared from spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) rats was used to test the hypothesis that impaired interactions between the gut microbiome and gut epithelium are involved and that these would be remediated with butyrate supplementation. Gene expressions in immune responses including antigen presentation and antiviral pathways were decreased in the gut epithelium of the SHR in organoids and confirmed in vivo; these deficits were corrected by butyrate supplementation. Deficits in gene expression driving epithelial proliferation and differentiation were also observed in SHR. These findings highlight the importance of aligned interactions of the gut microbiome and gut immune responses to blood pressure homeostasis.


Subject(s)
Colon/microbiology , Dysbiosis , Gastrointestinal Microbiome/physiology , Hypertension/microbiology , Animals , Butyrates/pharmacology , Colon/drug effects , Gastrointestinal Microbiome/drug effects , Male , Organoids , Rats , Rats, Inbred SHR , Rats, Inbred WKY , Transcriptome
19.
Am J Chin Med ; 49(2): 237-268, 2021.
Article in English | MEDLINE | ID: covidwho-1365230

ABSTRACT

Intestinal flora is essential for maintaining host health and plays a unique role in transforming Traditional Chinese Medicine (TCM). TCM, as a bodyguard, has saved countless lives and maintained human health in the long history, especially in this COVID-19 pandemic. Pains of diseases have been removed from the effective TCM therapy, such as TCM preparation, moxibustion, and acupuncture. With the development of life science and technology, the wisdom and foresight of TCM has been more displayed. Furthermore, TCM has been also inherited and developed in innovation to better realize the modernization and globalization. Nowadays, intestinal flora transforming TCM and TCM targeted intestinal flora treating diseases have been important findings in life science. More and more TCM researches showed the significance of intestinal flora. Intestinal flora is also a way to study TCM to elucidate the profound theory of TCM. Processing, compatibility, and properties of TCM are well demonstrated by intestinal flora. Thus, it is no doubt that intestinal flora is a core in TCM study. The interaction between intestinal flora and TCM is so crucial for host health. Therefore, it is necessary to sum up the latest results in time. This paper systematically depicted the profile of TCM and the importance of intestinal flora in host. What is more, we comprehensively summarized and discussed the latest progress of the interplay between TCM and intestinal flora to better reveal the core connotation of TCM.


Subject(s)
Drugs, Chinese Herbal/therapeutic use , Dysbiosis/microbiology , Gastrointestinal Microbiome , Medicine, Chinese Traditional , Autoimmune Diseases/microbiology , Autoimmune Diseases/therapy , COVID-19 , Cardiovascular Diseases/microbiology , Cardiovascular Diseases/therapy , Diabetes Mellitus/microbiology , Diabetes Mellitus/therapy , Electroacupuncture , Gastrointestinal Diseases/microbiology , Gastrointestinal Diseases/therapy , Humans , Metabolic Diseases/microbiology , Metabolic Diseases/therapy , Neoplasms/microbiology , Neoplasms/therapy , Non-alcoholic Fatty Liver Disease/microbiology , Non-alcoholic Fatty Liver Disease/therapy , Obesity/microbiology , Obesity/therapy , Renal Insufficiency, Chronic/microbiology , Renal Insufficiency, Chronic/therapy , SARS-CoV-2
20.
JCI Insight ; 6(20)2021 10 22.
Article in English | MEDLINE | ID: covidwho-1360585

ABSTRACT

In the COVID-19 pandemic, caused by SARS-CoV-2, many individuals experience prolonged symptoms, termed long-lasting COVID-19 symptoms (long COVID). Long COVID is thought to be linked to immune dysregulation due to harmful inflammation, with the exact causes being unknown. Given the role of the microbiome in mediating inflammation, we aimed to examine the relationship between the oral microbiome and the duration of long COVID symptoms. Tongue swabs were collected from patients presenting with COVID-19 symptoms. Confirmed infections were followed until resolution of all symptoms. Bacterial composition was determined by metagenomic sequencing. We used random forest modeling to identify microbiota and clinical covariates that are associated with long COVID symptoms. Of the patients followed, 63% developed ongoing symptomatic COVID-19 and 37% went on to long COVID. Patients with prolonged symptoms had significantly higher abundances of microbiota that induced inflammation, such as members of the genera Prevotella and Veillonella, which, of note, are species that produce LPS. The oral microbiome of patients with long COVID was similar to that of patients with chronic fatigue syndrome. Altogether, our findings suggest an association with the oral microbiome and long COVID, revealing the possibility that dysfunction of the oral microbiome may have contributed to this draining disease.


Subject(s)
COVID-19/complications , Dysbiosis , Inflammation , Microbiota , Aged , Bacteria/classification , Female , Gastrointestinal Microbiome , Humans , Male , Middle Aged , SARS-CoV-2
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