scholarly journals The Immune System through the Lens of Alcohol Intake and Gut Microbiota

2021 ◽  
Vol 22 (14) ◽  
pp. 7485
Author(s):  
Javier Calleja-Conde ◽  
Victor Echeverry-Alzate ◽  
Kora-Mareen Bühler ◽  
Pedro Durán-González ◽  
Jose Ángel Morales-García ◽  
...  

The human gut is the largest organ with immune function in our body, responsible for regulating the homeostasis of the intestinal barrier. A diverse, complex and dynamic population of microorganisms, called microbiota, which exert a significant impact on the host during homeostasis and disease, supports this role. In fact, intestinal bacteria maintain immune and metabolic homeostasis, protecting our organism against pathogens. The development of numerous inflammatory disorders and infections has been linked to altered gut bacterial composition or dysbiosis. Multiple factors contribute to the establishment of the human gut microbiota. For instance, diet is considered as one of the many drivers in shaping the gut microbiota across the lifetime. By contrast, alcohol is one of the many factors that disrupt the proper functioning of the gut, leading to a disruption of the intestinal barrier integrity that increases the permeability of the mucosa, with the final result of a disrupted mucosal immunity. This damage to the permeability of the intestinal membrane allows bacteria and their components to enter the blood tissue, reaching other organs such as the liver or the brain. Although chronic heavy drinking has harmful effects on the immune system cells at the systemic level, this review focuses on the effect produced on gut, brain and liver, because of their significance in the link between alcohol consumption, gut microbiota and the immune system.

2017 ◽  
Vol 474 (11) ◽  
pp. 1823-1836 ◽  
Author(s):  
Elizabeth Thursby ◽  
Nathalie Juge

The human gastrointestinal (GI) tract harbours a complex and dynamic population of microorganisms, the gut microbiota, which exert a marked influence on the host during homeostasis and disease. Multiple factors contribute to the establishment of the human gut microbiota during infancy. Diet is considered as one of the main drivers in shaping the gut microbiota across the life time. Intestinal bacteria play a crucial role in maintaining immune and metabolic homeostasis and protecting against pathogens. Altered gut bacterial composition (dysbiosis) has been associated with the pathogenesis of many inflammatory diseases and infections. The interpretation of these studies relies on a better understanding of inter-individual variations, heterogeneity of bacterial communities along and across the GI tract, functional redundancy and the need to distinguish cause from effect in states of dysbiosis. This review summarises our current understanding of the development and composition of the human GI microbiota, and its impact on gut integrity and host health, underlying the need for mechanistic studies focusing on host–microbe interactions.


2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Anshul Sinha ◽  
Corinne F. Maurice

The human gut is an extremely active immunological site interfacing with the densest microbial community known to colonize the human body, the gut microbiota. Despite tremendous advances in our comprehension of how the gut microbiota is involved in human health and interacts with the mammalian immune system, most studies are incomplete as they typically do not consider bacteriophages. These bacterial viruses are estimated to be as numerous as their bacterial hosts, with tremendous and mostly uncharacterized genetic diversity. In addition, bacteriophages are not passive members of the gut microbiota, as highlighted by the recent evidence for their active involvement in human health. Yet, how bacteriophages interact with their bacterial hosts and the immune system in the human gut remains poorly described. Here, we aim to fill this gap by providing an overview of bacteriophage communities in the gut during human development, detailing recent findings for their bacterial-mediated effects on the immune response and summarizing the latest evidence for direct interactions between them and the immune system. The dramatic increase in antibiotic-resistant bacterial pathogens has spurred a renewed interest in using bacteriophages for therapy, despite the many unknowns about bacteriophages in the human body. Going forward, more studies encompassing the communities of bacteria, bacteriophages, and the immune system in diverse health and disease settings will provide invaluable insight into this dynamic trio essential for human health.


Nanoscale ◽  
2021 ◽  
Author(s):  
Jiyan Qiao ◽  
Rui Chen ◽  
Mengjie Wang ◽  
Ru Bai ◽  
Xuejing Cui ◽  
...  

Exposure to micro/nanoplastics (M/NPLs) deteriorates the intestinal barrier by disturbing the bacterial composition in the gut.


2021 ◽  
Vol 12 ◽  
Author(s):  
Xubing Yuan ◽  
Junping Zheng ◽  
Lishi Ren ◽  
Siming Jiao ◽  
Cui Feng ◽  
...  

Glucosamine (GlcN) is used as a supplement for arthritis and joint pain and has been proved to have effects on inflammation, cancer, and cardiovascular diseases. However, there are limited studies on the regulatory mechanism of GlcN against glucose and lipid metabolism disorder. In this study, we treated high-fat diet (HFD)-induced diabetic mice with GlcN (1 mg/ml, in drinking water) for five months. The results show that GlcN significantly reduced the fasting blood glucose of HFD-fed mice and improved glucose tolerance. The feces of intestinal contents in mice were analyzed using 16s rDNA sequencing. It was indicated that GlcN reversed the imbalanced gut microbiota in HFD-fed mice. Based on the PICRUSt assay, the signaling pathways of glucolipid metabolism and biosynthesis were changed in mice with HFD feeding. By quantitative real-time PCR (qPCR) and hematoxylin and eosin (H&E) staining, it was demonstrated that GlcN not only inhibited the inflammatory responses of colon and white adipose tissues, but also improved the intestinal barrier damage of HFD-fed mice. Finally, the correlation analysis suggests the most significantly changed intestinal bacteria were positively or negatively related to the occurrence of inflammation in the colon and fat tissues of HFD-fed mice. In summary, our studies provide a theoretical basis for the potential application of GlcN to glucolipid metabolism disorder through the regulation of gut microbiota.


Author(s):  
Xing Heng ◽  
Yuanhe Jiang ◽  
Weihua Chu

Antibiotics which can treat or prevent infectious diseases play an important role in medical therapy. However, the use of antibiotics has potential negative effects on the health of the host. For example, antibiotics use may affect the host's immune system by altering the gut microbiota. Therefore, the aim of the study was to investigate the influence of antifungal (fluconazole) treatment on gut microbiota and immune system of mice. Results showed that gut microbial composition of mice receiving fluconazole treatment was significantly changed after the trial. Fluconazole did not affect the relative abundance of bacteria but significantly reduced the diversity of bacterial flora. In the Bacteriome, Firmicutes and Proteobacteria significantly increased, while Bacteroidetes, Deferribacteres, Patescibacteria, and Tenericutes showed a remarkable reduction in fluconazole treated group in comparison with the control group. In the mycobiome, the relative abundance of Ascomycota was significantly decreased and Mucoromycota was significantly increased in the intestine of mice treated with fluconazole compared to the control group. RT-qPCR results showed that the relative gene expression of ZO-1, occludin, MyD88, IL-1β, and IL-6 was decreased in fluconazole-treated group compared to the control. Serum levels of IL-2, LZM and IgM were significantly increased, while IgG level had considerably down-regulated in the fluconazole-treated compared to the control. These results suggest that the administration of fluconazole can influence the gut microbiota and that a healthy gut microbiome is important for the regulation of the host immune responses.


Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 927
Author(s):  
Paulina Trzeciak ◽  
Mariola Herbet

The intestinal microbiota plays an important role in the pathophysiology of depression. As determined, the microbiota influences the shaping and modulation of the functioning of the gut–brain axis. The intestinal microbiota has a significant impact on processes related to neurotransmitter synthesis, the myelination of neurons in the prefrontal cortex, and is also involved in the development of the amygdala and hippocampus. Intestinal bacteria are also a source of vitamins, the deficiency of which is believed to be related to the response to antidepressant therapy and may lead to exacerbation of depressive symptoms. Additionally, it is known that, in periods of excessive activation of stress reactions, the immune system also plays an important role, negatively affecting the tightness of the intestinal barrier and intestinal microflora. In this review, we have summarized the role of the gut microbiota, its metabolites, and diet in susceptibility to depression. We also describe abnormalities in the functioning of the intestinal barrier caused by increased activity of the immune system in response to stressors. Moreover, the presented study discusses the role of psychobiotics in the prevention and treatment of depression through their influence on the intestinal barrier, immune processes, and functioning of the nervous system.


Author(s):  
Xianglu Wang ◽  
Qiang Tang ◽  
Huiqin Hou ◽  
Wanru Zhang ◽  
Mengfan Li ◽  
...  

As a class of the commonly used drugs in clinical practice, non-steroidal anti-inflammatory drugs (NSAIDs) can cause a series of adverse events including gastrointestinal injuries. Besides upper gastrointestinal injuries, NSAID enteropathy also attracts attention with the introduction of capsule endoscopy and double balloon enteroscopy. However, the pathogenesis of NSAID enteropathy remains to be entirely clarified. Growing evidence from basic and clinical studies presents that gut microbiota is a critical factor in NSAID enteropathy progress. We have reviewed the recent data about the interplay between gut microbiota dysbiosis and NSAID enteropathy. The chronic medication of NSAIDs could change the composition of the intestinal bacteria and aggravate bile acids cytotoxicity. Meanwhile, NSAIDs impair the intestinal barrier by inhibiting cyclooxygenase and destroying mitochondria. Subsequently, intestinal bacteria translocate into the mucosa, and then lipopolysaccharide released from gut microbiota combines to Toll-like receptor 4 and induce excessive production of nitric oxide and pro-inflammatory cytokines. Intestinal injuries present in the condition of intestinal inflammation and oxidative stress. In this paper, we also have reviewed the possible strategies of regulating gut microbiota for the management of NSAID enteropathy, including antibiotics, probiotics, prebiotics, mucosal protective agents, and fecal microbiota transplant, and we emphasized the adverse effects of proton pump inhibitors on NSAID enteropathy. Therefore, this review will provide new insights into a better understanding of gut microbiota in NSAID enteropathy.


Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3039
Author(s):  
Juan Salazar ◽  
Lissé Angarita ◽  
Valery Morillo ◽  
Carla Navarro ◽  
María Sofía Martínez ◽  
...  

Diabetes Mellitus (DM) is an inflammatory clinical entity with different mechanisms involved in its physiopathology. Among these, the dysfunction of the gut microbiota stands out. Currently, it is understood that lipid products derived from the gut microbiota are capable of interacting with cells from the immune system and have an immunomodulatory effect. In the presence of dysbiosis, the concentration of lipopolysaccharides (LPS) increases, favoring damage to the intestinal barrier. Furthermore, a pro-inflammatory environment prevails, and a state of insulin resistance and hyperglycemia is present. Conversely, during eubiosis, the production of short-chain fatty acids (SCFA) is fundamental for the maintenance of the integrity of the intestinal barrier as well as for immunogenic tolerance and appetite/satiety perception, leading to a protective effect. Additionally, it has been demonstrated that alterations or dysregulation of the gut microbiota can be reversed by modifying the eating habits of the patients or with the administration of prebiotics, probiotics, and symbiotics. Similarly, different studies have demonstrated that drugs like Metformin are capable of modifying the composition of the gut microbiota, promoting changes in the biosynthesis of LPS, and the metabolism of SCFA.


2013 ◽  
Vol 4 (1) ◽  
pp. 31-37 ◽  
Author(s):  
M. Rothe ◽  
M. Blaut

Diet is a major force that shapes the composition and activity of the gut microbiota. This is evident from alterations in gut microbiota composition after weaning or drastic dietary changes. Owing to the complexity of the microbiota, interactions of intestinal bacteria with the host are difficult to study. Gnotobiotic animal models offer the opportunity to reduce the complexity and the interindividual variability of the intestinal microbiota. Germ-free animals were associated with a simplified microbial community consisting of eight bacterial species, that are found in the human gut. These microbes were selected because their genome sequences are available, and they mimic to some extent the metabolic activity of the human gut microbiota. The microbiota responded to dietary modifications by changes in the relative proportions of the community members. This model offers the chance to better define the role of intestinal bacteria in obesity development, but little is known on how diet affects intestinal bacteria at the cellular level. Mice monoassociated with Escherichia coli were used as a simplified model to investigate the influence of dietary factors on bacterial protein expression in the intestine. The mice were fed three different diets: a carbohydrate (lactose)-rich diet, a protein-rich diet and a diet rich in starch. The lactose-rich diet led to an induction of proteins involved in E. coli's oxidative stress response (Fur, AhpF, Dps). The corresponding genes are under control of the OxyR transcriptional regulator which is activated by oxidative stress. Further experiments demonstrated that osmotic stress exerted by various carbohydrates leads to an upregulation of proteins belonging to the oxyR regulon. The data suggest that the upregulated proteins enable intestinal E. coli to better cope with diet-induced osmotic stress. These examples demonstrate that gnotobiotic animal models are a valuable tool for studying diet-induced changes at the community and the cell level.


Immunity ◽  
2014 ◽  
Vol 40 (6) ◽  
pp. 815-823 ◽  
Author(s):  
Philip P. Ahern ◽  
Jeremiah J. Faith ◽  
Jeffrey I. Gordon

Sign in / Sign up

Export Citation Format

Share Document