BACTERIAL TRANSLOCATION: MICROBIOTA-INTESTINE-LUNG AXIS AND PRO-INFLAMMATORY STATUS IN THE SEVERITY OF COVID-19

Although severe acute respiratory syndrome coronavirus – 2 (SARS-CoV-2), causing coronavirus disease 2019 (COVID-19) pandemic, is primarily associated with a respiratory infection, it has also been linked to multisystem involvement that includes the digestive tract. Gastrointestinal (GI) manifestations are common in patients with COVID-19 due to the high viral load lodged in the small intestine's mucosa. As a result, it causes an increase in the permeability of the intestinal barrier that favours the passage and translocation of bacteria, from the lumen of the intestine, towards the internal environment, with the appearance of sepsis, with evidence that SARS-CoV-2 has been found in faeces. This article highlights epidemiology, clinical symptoms, and mechanisms related to manifestations of disease in the GI tract and its pathogenesis in patients with COVID-19. It highlights bacterial translocation and COVID-19, mechanisms that control bacterial translocation, intestinal infection and feco-oral transmission, defense

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TRANSLOCATION OF INTESTINAL MICROFLORA IN CIRRHOSIS

Hepatology and Gastroenterology ◽

10.25298/2616-5546-2020-4-2-143-150 ◽

2020 ◽

Vol 4 (2) ◽

pp. 143-150

Author(s):

D. I. Haurylenka ◽

◽

N. N. Silivontchik ◽

Keyword(s):

Bacterial Translocation ◽

Bacterial Infections ◽

Intestinal Microflora ◽

Intestinal Barrier ◽

Intestinal Bacteria ◽

Cochrane Collaboration ◽

Russian Language ◽

Intestinal Lumen ◽

Future Research ◽

Inflammatory Status

Background. Understanding of intestinal bacteria-host interaction physiology as well as bacterial translocation characteristics at the initial stages and in advanced cirrhosis emphasizes the importance of approaches minimizing the migration of microorganisms and their components from the intestinal lumen. Objective – to provide a brief review of publications highlighting the problem of bacterial intestinal translocation as the main mechanism for the development of bacterial infections and pro-inﬂammatory status in patients with liver cirrhosis. Material and methods. We performed the study and analysis of English- and Russian-language articles over the past 30 years contained in the following databases: PubMed, Cochrane Collaboration, UpToDate. The key words were: «intestinal microﬂora translocation», «bacterial translocation», «translocation markers». Results. Contemporary views on changes of the intestinal barrier and those of innate and adaptive immunity systems in liver diseases are considered. Data on possibility and signifcance of detecting bacterial translocation are presented.Current methods used for gut microbiome analysis as well as some areas for future research are discussed. Conclusion. A validated marker/markers is required to study bacterial translocation in cirrhosis.

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Significance of nucleic acid positive anal swab in COVID-19 patients

Open Medicine ◽

10.1515/med-2021-0236 ◽

2021 ◽

Vol 16 (1) ◽

pp. 332-337

Author(s):

Xiaoli Li ◽

Lei Rong ◽

Peiyan Zhang ◽

Jian Xu ◽

Yan Rong

Keyword(s):

Platelet Count ◽

Clinical Symptoms ◽

Influence Factors ◽

Recovery Phase ◽

Negative Group ◽

Pharyngeal Swab ◽

Positive Group ◽

Oral Transmission ◽

Significant Difference ◽

Anal Swab

Abstract Aim We compared the clinical characteristics of patients with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) positive and negative anal swabs during coronavirus disease 2019 (COVID-19) recovery and investigated the clinical significance and influence factors of anal swab detection. Methods This study retrospectively analyzed 23 moderate COVID-19 patients in the recovery phase. They were divided into anal swab positive group (n = 13) (negative for pharyngeal swabs but positive for anal swabs) and anal swab negative group (n = 10) (negative for pharyngeal and anal swabs). The epidemiology, clinical symptoms, time of pharyngeal swabs turning negative, and laboratory results were compared. Results The time of pharyngeal swabs turning negative in the anal swab positive group was 6 (5–8.5) days, significantly longer than that in the anal swab negative group (1 (1–4.25) days), P = 0.0002). The platelet count of the anal swab positive group was significantly lower than that of the anal swab negative group (198 (135–235) × 109/L vs 240.5 (227–264.75) × 109/L, P = 0.0248). No significant difference was observed between the two groups in other variables. Conclusions The time of pharyngeal swab turning negative in anal swab positive patients is longer than that in anal swab negative patients. The platelet count can be used as an indicator for viral infection evaluation. For patients with a longer time of pharyngeal swabs turning negative, the combined testing of the anal swab and platelet counts may help to avoid pharyngeal swab false negatives, premature discharge, and the possibility of fecal-oral transmission.

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The DNA Sensor AIM2 Protects against Streptozotocin-Induced Type 1 Diabetes by Regulating Intestinal Homeostasis via the IL-18 Pathway

Cells ◽

10.3390/cells9040959 ◽

2020 ◽

Vol 9 (4) ◽

pp. 959 ◽

Cited By ~ 2

Author(s):

Jefferson Antônio Leite ◽

Gabriela Pessenda ◽

Isabel C. Guerra-Gomes ◽

Alynne Karen Mendonça de Santana ◽

Camila André Pereira ◽

...

Keyword(s):

Type 1 Diabetes ◽

Gut Microbiota ◽

Bacterial Translocation ◽

Intestinal Barrier ◽

Intestinal Barrier Function ◽

Dna Sensor ◽

Proinflammatory Response

Pattern recognition receptors (PRRs), such as Nod2, Nlrp3, Tlr2, Trl4, and Tlr9, are directly involved in type 1 diabetes (T1D) susceptibility. However, the role of the cytosolic DNA sensor, AIM2, in T1D pathogenesis is still unknown. Here, we demonstrate that C57BL/6 mice lacking AIM2 (AIM2−/−) are prone to streptozotocin (STZ)-induced T1D, compared to WT C57BL/6 mice. The AIM2−/− mice phenotype is associated with a greater proinflammatory response in pancreatic tissues, alterations in gut microbiota and bacterial translocation to pancreatic lymph nodes (PLNs). These alterations are related to an increased intestinal permeability mediated by tight-junction disruption. Notably, AIM2−/− mice treated with broad-spectrum antibiotics (ABX) are protected from STZ-induced T1D and display a lower pancreatic proinflammatory response. Mechanistically, the AIM2 inflammasome is activated in vivo, leading to an IL-18 release in the ileum at 15 days after an STZ injection. IL-18 favors RegIIIγ production, thus mitigating gut microbiota alterations and reinforcing the intestinal barrier function. Together, our findings show a regulatory role of AIM2, mediated by IL-18, in shaping gut microbiota and reducing bacterial translocation and proinflammatory response against insulin-producing β cells, which ultimately results in protection against T1D onset in an STZ-induced diabetes model.

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Confirmation and Prevention of Intestinal Barrier Dysfunction and Bacterial Translocation Caused by Methotrexate

Digestive Diseases and Sciences ◽

10.1007/s10620-005-9058-0 ◽

2006 ◽

Vol 51 (9) ◽

pp. 1549-1556 ◽

Cited By ~ 21

Author(s):

Desheng Song ◽

Bin Shi ◽

Hua Xue ◽

Yousheng Li ◽

Xiaodong Yang ◽

...

Keyword(s):

Bacterial Translocation ◽

Intestinal Barrier ◽

Barrier Dysfunction ◽

Intestinal Barrier Dysfunction

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Integrity of the Intestinal Barrier: The Involvement of Epithelial Cells and Microbiota—A Mutual Relationship

Animals ◽

10.3390/ani12020145 ◽

2022 ◽

Vol 12 (2) ◽

pp. 145

Author(s):

Małgorzata Gieryńska ◽

Lidia Szulc-Dąbrowska ◽

Justyna Struzik ◽

Matylda Barbara Mielcarska ◽

Karolina Paulina Gregorczyk-Zboroch

Keyword(s):

Epithelial Cells ◽

Gut Microbiota ◽

Metabolic Diseases ◽

Intestinal Barrier ◽

Intercellular Junctions ◽

Gi Tract ◽

First Line ◽

Mucosal Integrity ◽

Physical Defense ◽

Mutualistic Relationship

The gastrointestinal tract, which is constantly exposed to a multitude of stimuli, is considered responsible for maintaining the homeostasis of the host. It is inhabited by billions of microorganisms, the gut microbiota, which form a mutualistic relationship with the host. Although the microbiota is generally recognized as beneficial, at the same time, together with pathogens, they are a permanent threat to the host. Various populations of epithelial cells provide the first line of chemical and physical defense against external factors acting as the interface between luminal microorganisms and immunocompetent cells in lamina propria. In this review, we focus on some essential, innate mechanisms protecting mucosal integrity, thus responsible for maintaining intestine homeostasis. The characteristics of decisive cell populations involved in maintaining the barrier arrangement, based on mucus secretion, formation of intercellular junctions as well as production of antimicrobial peptides, responsible for shaping the gut microbiota, are presented. We emphasize the importance of cross-talk between gut microbiota and epithelial cells as a factor vital for the maintenance of the homeostasis of the GI tract. Finally, we discuss how the imbalance of these regulations leads to the compromised barrier integrity and dysbiosis considered to contribute to inflammatory disorders and metabolic diseases.

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Change of Intestinal Microbiome in Patients with Coronavirus Infection

Ukraïnsʹkij žurnal medicini bìologìï ta sportu ◽

10.26693/jmbs06.05.022 ◽

2021 ◽

Vol 6 (5) ◽

pp. 22-27

Author(s):

M. M. Mishina ◽

◽

O. V. Kotsar ◽

Pochernina M. H. ◽

O. V. Kochnieva ◽

...

Keyword(s):

Bacterial Translocation ◽

Intestinal Barrier ◽

Multiple Organ ◽

Infection Process ◽

The Body ◽

Intestinal Microbiome ◽

Intestinal Lumen ◽

Treatment Regimens ◽

Analysis And Synthesis ◽

Coronavirus Infection

The purpose of the study was to analyze modern literature on the problems of dysbiosis in patients with COVID-19, to study the main mechanisms of systemic interaction between the intestine and lungs, as well as changes in the microbiota that occur under the influence of coronavirus infection. Materials and methods. A comprehensive selection of research methods was used for the work: systematization of the material, the method of generalization, methods of analysis and synthesis. Scientific works in the field of microbiology, epidemiology and infectious diseases were studied. Literature data for the last 2 years (2019-2021) were considered. The results of bacteriological studies from patients with COVID infection were described. The data obtained were processed using information-analytical and statistical-analytical methods. Results and discussion. As a result of this work, a complex of connections between intestine and lungs, which is called the "intestinal-lung axis", was considered. It is known that the interaction between these two biotopes occurs with the participation of microflora and its metabolites. Dysfunction of the intestinal barrier is accompanied by bacterial translocation. Bacteria from the intestinal lumen enter the liver through the portal vein system. The lymphatic pathway of bacterial translocation from the intestine to the lungs is also possible, which causes multiple organ failure syndrome in coronavirus infection. The COVID-19 virus is able to reduce the number of ACE2 receptors in the gastrointestinal tract, which leads to an imbalance in the intestines. At the same time, the infection process in the lungs promotes the growth of bacteria of the Enterobacteriacae family in the intestine, which also leads to dysbiotic disorders. The use of probiotics is an effective tool in the complex treatment of this infection, which facilitates the general condition of patients. In the course of treatment, it is important not only to eliminate the virus from the body, but also to restore normal intestinal microbiota after an infection. Conclusion. Thus, the use of probiotic drugs for the treatment of patients with coronavirus infection can significantly reduce the risk of developing dysbiosis and improve the condition of patients. A perspective direction is the development of new treatment regimens for dysbiotic conditions using probiotics, eubiotics, synbiotics and postbiotics to prevent the development of severe complications in COVID infection

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Simvastatin improves the prognosis of endotoxin-induced disseminated intravascular coagulation by regulating the intestinal microenvironment

10.21203/rs.3.rs-76982/v1 ◽

2020 ◽

Author(s):

Min Xu ◽

Lili Luo ◽

Mengyi Du ◽

Lu Tang ◽

Jie Zhou ◽

...

Keyword(s):

Bacterial Translocation ◽

Disseminated Intravascular Coagulation ◽

Intestinal Barrier ◽

Plasminogen Activator Inhibitor ◽

Coagulation Factors ◽

Organ Damage ◽

Multiple Organ ◽

Plasminogen Activator Inhibitor 1 ◽

Intravascular Coagulation ◽

Coagulation Dysfunction

Abstract Background: Disseminated intravascular coagulation (DIC) is characterized by extensive endothelial injury and coagulation activation that is primarily caused by infection and can be aggravated by the gut due to increased permeability and bacterial translocation. Studies have shown that statins play an important role in reducing inflammation, protecting the endothelium and improving coagulation. In addition, statins regulate tight junction (TJ) proteins and gut microbes. Therefore, we aimed to investigate whether simvastatin improves DIC prognosis by regulating the intestinal microenvironment. Methods: Mice were administered 20 mg/kg simvastatin by gavage for 2 weeks and then intraperitoneally injected with 50 mg/kg endotoxin. Twelve hours later, cytokine release, coagulation dysfunction, multiple organ damage and survival were assessed. In addition, intestinal barrier and permeability and bacteria and bacteria translocation were evaluated. Results: We found that the severity of endotoxin-induced DIC was significantly improved in simvastatin-pretreated mice, who showed attenuated depletion of coagulation factors and platelets, decreased plasminogen activator inhibitor-1 (PAI-1) expression, reduced organ fibrin deposition and an improved survival rate. In addition, simvastatin reduced epithelial apoptosis, increased TJ gene expression, and upregulated antimicrobial peptides, lysozyme and mucins. Simvastatin-pretreated mice showed increased Lactobacillales counts, while the LPS group had increased numbers of Desulfovibrio and Mucispirillum, which produce harmful toxins and damage the intestinal epithelium and mucosa. Finally, with the decreased intestinal permeability in the simvastatin group, bacterial translocation in the organs and blood was significantly reduced, both in quantity and species. Conclusions: Simvastatin improves DIC prognosis, and the intestinal microenvironment participates in this process.

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Introduction

ESC CardioMed ◽

10.1093/med/9780198784906.003.0262_update_001 ◽

2018 ◽

pp. 1081-1082

Author(s):

Gerhard Rogler

Keyword(s):

Heart Failure ◽

Heart Disease ◽

Chronic Heart Failure ◽

Bacterial Translocation ◽

Gastrointestinal Disease ◽

Intestinal Barrier ◽

Mucosal Barrier ◽

Intestinal Barrier Function ◽

Oral Drug ◽

Intestinal Microcirculation

Gastrointestinal disease and heart disease seem to be two groups of diseases that do not have much in common. However, recent insights have changed this assumption: the intestine’s basic functions, digestion and absorption, are obviously clinically relevant for almost all oral drug treatments of diseases. An impairment of intestinal barrier function is followed by increased bacterial translocation across the intestinal mucosa leading to increased levels of circulating bacteria and bacterial products. This is assumed to be associated with atherosclerosis and chronic heart failure. Vice versa, an impaired cardiac function in the setting of chronic heart failure may lead to a defect in the mucosal barrier and increased bacterial translocation via changes in intestinal microcirculation. In addition, recent evidence indicates that conditions such as metabolic syndrome or obesity—certainly risk factors for heart disease—are influenced by intestinal microbiota composition.

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Effects of Synbiotics to Prevent Postoperative Infectious Complications in Highly Invasive Abdominal Surgery

Annals of Nutrition and Metabolism ◽

10.1159/000479920 ◽

2017 ◽

Vol 71 (Suppl. 1) ◽

pp. 23-30 ◽

Cited By ~ 2

Author(s):

Yukihiro Yokoyama ◽

Takashi Asahara ◽

Koji Nomoto ◽

Masato Nagino

Keyword(s):

Lactic Acid ◽

Abdominal Surgery ◽

Bacterial Translocation ◽

Barrier Function ◽

Intestinal Microflora ◽

Surgical Stress ◽

Controlled Trial ◽

Intestinal Barrier ◽

Short Chain Fatty Acids ◽

Intestinal Barrier Function

Postoperative infectious complication (POIC) is one of the most common complications following highly invasive abdominal surgeries, such as hepatectomy, esophagectomy, and pancreatoduodenectomy. The surgical stress temporarily deteriorates the intestinal microenvironment, and the fecal concentrations of beneficial bacteria such as Bifidobacterium and Lactobacillus decrease following highly invasive abdominal surgery. In parallel with these changes, the concentrations of fecal short-chain fatty acids (SCFAs) such as acetic acid, propionic acid, and butyric acid also decrease after surgery. In contrast, the fecal concentration of lactic acid increases under this condition because of the deterioration of the metabolism from lactic acid to SCFAs by normal intestinal microflora. Decreased fecal concentration of SCFAs may lead to an impaired intestinal barrier function under stressful condition. Translocation of bacteria from the gut to lymphatic and bloodstream leads to bacteremia and subsequent POICs. The incidence of POICs in patients with unhealthy intestinal microflora before surgery may be more because their intestine is more susceptible to bacterial translocation induced by surgical stress. Therefore, improving the intestinal microenvironment and intestinal barrier function before surgery is crucial to prevent POICs following highly invasive abdominal surgeries. In this regard, the use preoperative synbiotics therapy may be one of the effective ways because it has been shown to improve intestinal microflora, increase fecal SCFAs, prevent bacterial translocation, and reduce the incidence of POICs in several randomized controlled trial in patients undergoing highly invasive abdominal surgeries.

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