scholarly journals Implication of Gut Microbiota in Cardiovascular Diseases

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Wenyi Zhou ◽  
Yiyu Cheng ◽  
Ping Zhu ◽  
M. I. Nasser ◽  
Xueyan Zhang ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiovascular Diseases ◽  
Programmed Cell Death ◽  
Gut Microbiota ◽  
Intestinal Flora ◽  
Short Chain Fatty Acids ◽  
Secondary Bile Acid ◽  
Cardiac Disorders ◽  
The Relationship

Emerging evidence has identified the association between gut microbiota and various diseases, including cardiovascular diseases (CVDs). Altered intestinal flora composition has been described in detail in CVDs, such as hypertension, atherosclerosis, myocardial infarction, heart failure, and arrhythmia. In contrast, the importance of fermentation metabolites, such as trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), and secondary bile acid (BA), has also been implicated in CVD development, prevention, treatment, and prognosis. The potential mechanisms are conventionally thought to involve immune regulation, host energy metabolism, and oxidative stress. However, numerous types of programmed cell death, including apoptosis, autophagy, pyroptosis, ferroptosis, and clockophagy, also serve as a key link in microbiome-host cross talk. In this review, we introduced and summarized the results from recent studies dealing with the relationship between gut microbiota and cardiac disorders, highlighting the role of programmed cell death. We hope to shed light on microbiota-targeted therapeutic strategies in CVD management.

scholarly journals Reduced fecal short-chain fatty acids levels and the relationship with gut microbiota in IgA nephropathy

2021 ◽  
Author(s):  
Lingxiong Chai ◽  
Qun Luo ◽  
Kedan Cai ◽  
Kaiyue Wang ◽  
Binbin Xu
Keyword(s):  
Gut Microbiota ◽  
Iga Nephropathy ◽  
Butyric Acid ◽  
Intestinal Flora ◽  
Short Chain Fatty Acids ◽  
Caproic Acid ◽  
Isobutyric Acid ◽  
Control Group ◽  
Β Diversity

Abstract Background: IgA nephropathy(IgAN)) is the common pathological type of glomerular diseases. The role of gut microbiota in mediating "gut-IgA nephropathy" has not received sufficient attention in the previous studies. The purpose of this study was to investigate the changes of fecal short-chain fatty acids(SCFAs), a metabolite of the intestinal microbiota, in patients with IgAN and its correlation with intestinal flora and clinical indicators, and to further investigate the role of the gut-renal axis in IgAN.Methods: There were 29 patients with IgAN and 29 normal control subjects recruited from January 2018 to May 2018. The fresh feces were collected. The fecal SCFAs were measured by gas chromatography/mass spectrometry and gut microbiota was analysed by16S rDNA sequences, followed by estimation of α- and β-diversity. Correlation analysis was performed using the spearman’s correlation test between SCFAs and gut microbiota. Results:The levels of acetic acid, propionic acid, butyric acid, isobutyric acid and caproic acid in the IgAN patients were significantly reduced compared with control group(P<0.05). Butyric acid(r=-0.336, P=0.010) and isobutyric acid(r=-0.298, P=0.022) were negatively correlated with urea acid; butyric acid(r=-0.316, P=0.016) was negatively correlated with urea nitrogen; caproic acid(r=-0.415,P=0.025) showed negative correlation with 24-h urine protein level.Exemplified by the results of α-diversity and β-diversity, the intestinal flora of IgAN patients was significantly different from that of the control group. Acetic acid was positively associated with c_Clostridia(r=0.357, P=0.008), o_Clostridiales(r=0.357, P=0.008) and g_Eubacterium_coprostanoligenes_group(r=0.283, P=0.036). Butyric acid was positively associated with g_Alistipes (r=0.278, P=0.040). The relative abundance of those were significantly decreased in IgAN group compared to control group.Conclusion: The levels of fecal SCFAs in the IgAN patients were reduced, and correlated with clinical parameters and gut microbiota, which may be involved in the pathogenesis of IgAN, and this finding may provide a new therapeutic approach.

scholarly journals Bcl2 inhibits apoptosis associated with terminal differentiation of HL- 60 myeloid leukemia cells

Blood ◽  
1994 ◽  
Vol 83 (8) ◽  
pp. 2261-2267 ◽  
Author(s):  
L Naumovski ◽  
ML Cleary
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Myeloid Cells ◽  
Terminal Differentiation ◽  
Retroviral Gene Transfer ◽  
Protein Levels ◽  
All Trans Retinoic Acid ◽  
Bcl2 Protein ◽  
The Relationship

Abstract The Bcl2 protein inhibits apoptosis (programmed cell death) induced by a variety of noxious stimuli. However, relatively little is known about its effect on apoptosis that occurs after terminal differentiation. Bcl2 protein levels decrease during differentiation of myeloid cells into granulocytes that subsequently undergo apoptosis, but the potential role of Bcl2 in coupling survival and differentiation remains undefined. To ascertain the relationship between decreasing Bcl2 levels and the onset of apoptosis in differentiating myeloid cells, Bcl2 was hyperexpressed in the HL-60 cell line after retroviral gene transfer. After treatment of HL-60/BCL2 cells with all-trans retinoic acid or phorbol myristic acid, Bcl2 levels did not decrease as in normal HL-60 cells but, rather, increased because of activation of the viral promoter. Differentiation of the Bcl2-overexpressing cells was similar to that of normal HL-60 cells, but they showed little evidence for apoptosis and had a prolonged survival. These studies show that the survival-enhancing properties of Bcl2 counteract programmed cell death that accompanies terminal differentiation; however, Bcl2 has no significant effect on differentiation itself, suggesting that apoptosis and differentiation are regulated independently in myeloid cells.

scholarly journals Role of Gut Microbiota in the Pathogenesis of Cardiovascular Diseases and Metabolic Syndrome

2018 ◽  
Vol 14 (4) ◽  
pp. 567-574 ◽  
Author(s):  
O. M. Drapkina ◽  
O. E. Shirobokikh
Keyword(s):  
Heart Failure ◽  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Cardiovascular Diseases ◽  
Gut Microbiota ◽  
Bile Acids ◽  
G Protein ◽  
Short Chain Fatty Acids ◽  
Short Chain

The role of gut microbiota in the pathogenesis of cardiovascular diseases (CVD) and metabolic syndrome has attracted massive attention in the past decade. Accumulating evidence has revealed that the metabolic potential of gut microbiota can be identified as a contributing factor in the development of atherosclerosis, hypertension, heart failure, obesity, diabetes mellitus. The gut-host interaction occurs through many pathways including trimethylamine-N-oxide pathway (TMAO), short-chain fatty acids and second bile acids pathways. TMAO (the hepatic oxidation product of the microbial metabolite of trimethylamine) enhances platelet hyperreactivity and thrombosis risk and predicts major adverse cardiovascular events. Short-chain fatty acids and second bile acids, which are produced with the help of microbiota, can modulate host lipid metabolism as well as carbohydrate metabolism through several receptors such as G-protein-coupled receptors 41,43, farnesoid X-receptor, Takeda-G-protein-receptor-5. This way microbiota can impact host lipid levels, processes of weight gain, insulin sensitivity. Besides these metabolism-dependent pathways, there are some other pathways, which link microbiota and the pathogenesis of CVD. For example, lipopolysaccharide, the major component of the outer bacterial membrane, causes metabolic endotoxemia and low-grade systemic inflammation and contribute this way to obesity and progression of heart failure and atherosclerosis. This review aims to illustrate the complex interplay between microbiota, their metabolites, and the development and progression of CVD and metabolic syndrome. It is also discussed how modulating of gut microbiota composition and function through diet, prebiotics, probiotics and fecal microbiota transplantation can become a novel therapeutic and preventative target for CVD and metabolic syndrome. Many questions remain unresolved in this field and undoubtedly further studies are needed.

scholarly journals Reduced fecal short-chain fatty acids levels and the relationship with gut microbiota in IgA nephropathy

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Lingxiong Chai ◽  
Qun Luo ◽  
Kedan Cai ◽  
Kaiyue Wang ◽  
Binbin Xu
Keyword(s):  
Gut Microbiota ◽  
Iga Nephropathy ◽  
Butyric Acid ◽  
Intestinal Flora ◽  
Short Chain Fatty Acids ◽  
Caproic Acid ◽  
Isobutyric Acid ◽  
Control Group ◽  
Β Diversity

Abstract Background IgA nephropathy(IgAN)) is the common pathological type of glomerular diseases. The role of gut microbiota in mediating “gut-IgA nephropathy” has not received sufficient attention in the previous studies. The purpose of this study was to investigate the changes of fecal short-chain fatty acids(SCFAs), a metabolite of the intestinal microbiota, in patients with IgAN and its correlation with intestinal flora and clinical indicators, and to further investigate the role of the gut-renal axis in IgAN. Methods There were 29 patients with IgAN and 29 normal control subjects recruited from January 2018 to May 2018. The fresh feces were collected. The fecal SCFAs were measured by gas chromatography/mass spectrometry and gut microbiota was analysed by16S rDNA sequences, followed by estimation of α- and β-diversity. Correlation analysis was performed using the spearman’s correlation test between SCFAs and gut microbiota. Results The levels of acetic acid, propionic acid, butyric acid, isobutyric acid and caproic acid in the IgAN patients were significantly reduced compared with control group(P < 0.05). Butyric acid(r=-0.336, P = 0.010) and isobutyric acid(r=-0.298, P = 0.022) were negatively correlated with urea acid; butyric acid(r=-0.316, P = 0.016) was negatively correlated with urea nitrogen; caproic acid(r=-0.415,P = 0.025) showed negative correlation with 24-h urine protein level.Exemplified by the results of α-diversity and β-diversity, the intestinal flora of IgAN patients was significantly different from that of the control group. Acetic acid was positively associated with c_Clostridia(r = 0.357, P = 0.008), o_Clostridiales(r = 0.357, P = 0.008) and g_Eubacterium_coprostanoligenes_group(r = 0.283, P = 0.036). Butyric acid was positively associated with g_Alistipes (r = 0.278, P = 0.040). The relative abundance of those were significantly decreased in IgAN group compared to control group. Conclusions The levels of fecal SCFAs in the IgAN patients were reduced, and correlated with clinical parameters and gut microbiota, which may be involved in the pathogenesis of IgAN, and this finding may provide a new therapeutic approach.

Fecal Microbiota Transplantation (FMT) Alleviates Ovalbumin-induced Allergic Airway Inflammation in Neonatal Mice via the PD-1/PD-L1 Axis

2021 ◽  
Author(s):  
Cheng Wu ◽  
Juan Zhang ◽  
Yuan-Yuan Jia ◽  
Xing-Zhi Wang ◽  
Qiu-hong Li ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Mouse Model ◽  
Gut Microbiota ◽  
Airway Inflammation ◽  
Fecal Microbiota Transplantation ◽  
Allergic Airway Inflammation ◽  
Fecal Microbiota ◽  
Cell Death Protein

Abstract Asthma is the common respiratory disorder in children, which is associated with abnormal gut microbiota. Fecal microbiota transplantation (FMT) has successfully ameliorated the symptoms of several diseases and restored the balance of gut microbiota. However, there are few researches about the role of FMT in asthma. This study aimed at exploring whether FMT can alleviate allergic airway inflammation in neonatal mice and elucidating the probable underlying mechanism. A neonatal mouse model of ovalbumin (OVA)-induced allergic asthma was established and transplanted with fecal filtrates. Our results manifested that FMT could protect against the allergic airway inflammation through enhancing mesenteric CD11c + CD103 + DCs and accumulating mucosal Helios + Tregs. Besides, the programmed cell death protein 1/programmed cell death protein 1 ligand (PD-1/PD-L1) signal pathway was inhibited after FMT intervention. Furthermore, this beneficial role of FMT was also associated with the rebalanced gut microbiota, such as Akkermansia. Thus, our findings indicated that FMT intervention could exert a therapeutic effect in a neonatal mouse model of OVA-induced allergic airway inflammation through its remodeling on gut microbiota and regulation of Treg homeostasis via the PD-1/PD-L1 axis, which might be used as an alternative therapy for allergic asthma.

scholarly journals Bcl2 inhibits apoptosis associated with terminal differentiation of HL- 60 myeloid leukemia cells

Blood ◽  
1994 ◽  
Vol 83 (8) ◽  
pp. 2261-2267 ◽  
Author(s):  
L Naumovski ◽  
ML Cleary
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Myeloid Cells ◽  
Terminal Differentiation ◽  
Retroviral Gene Transfer ◽  
Protein Levels ◽  
All Trans Retinoic Acid ◽  
Bcl2 Protein ◽  
The Relationship

The Bcl2 protein inhibits apoptosis (programmed cell death) induced by a variety of noxious stimuli. However, relatively little is known about its effect on apoptosis that occurs after terminal differentiation. Bcl2 protein levels decrease during differentiation of myeloid cells into granulocytes that subsequently undergo apoptosis, but the potential role of Bcl2 in coupling survival and differentiation remains undefined. To ascertain the relationship between decreasing Bcl2 levels and the onset of apoptosis in differentiating myeloid cells, Bcl2 was hyperexpressed in the HL-60 cell line after retroviral gene transfer. After treatment of HL-60/BCL2 cells with all-trans retinoic acid or phorbol myristic acid, Bcl2 levels did not decrease as in normal HL-60 cells but, rather, increased because of activation of the viral promoter. Differentiation of the Bcl2-overexpressing cells was similar to that of normal HL-60 cells, but they showed little evidence for apoptosis and had a prolonged survival. These studies show that the survival-enhancing properties of Bcl2 counteract programmed cell death that accompanies terminal differentiation; however, Bcl2 has no significant effect on differentiation itself, suggesting that apoptosis and differentiation are regulated independently in myeloid cells.

scholarly journals Exploring the Emerging Role of the Gut Microbiota and Tumor Microenvironment in Cancer Immunotherapy

2021 ◽  
Vol 11 ◽  
Author(s):  
Qin Qiu ◽  
Yuqi Lin ◽  
Yucui Ma ◽  
Xiaoling Li ◽  
Juan Liang ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Microenvironment ◽  
Programmed Cell Death ◽  
Gut Microbiota ◽  
Cancer Immunotherapy ◽  
Cytotoxic T Lymphocyte ◽  
Immune Surveillance ◽  
Host Immune System ◽  
The Impact

The tumor microenvironment (TME) is a complex ecosystem, which includes many different types of cells, abnormal vascular systems, and immunosuppressive cytokines. TME serves an important function in tumor tolerance and escapes from immune surveillance leading to tumor progression. Indeed, there is increasing evidence that gut microbiome is associated with cancer in a variety of ways, as specific microbial signatures are known to promote cancer development and influence safety, tolerability, and efficacy of therapies. Studies over the past five years have shown that the composition of the intestinal microbiota has a significant impact on the efficacy of anticancer immunosurveillance, which contribute to the therapeutic activity of cancer immunotherapies based on targeting cytotoxic T lymphocyte protein 4 (CTLA-4) or programmed cell death protein 1 (PD-1)–programmed cell death 1 ligand 1 (PD-L1) axis. In this review, we mainly discuss the impact of TME on cancer and immunotherapy through immune-related mechanisms. We subsequently discuss the influence of gut microbiota and its metabolites on the host immune system and the formation of TME. In addition, this review also summarizes the latest research on the role of gut microbiota in cancer immunotherapy.

The Food-gut Human Axis: The Effects of Diet on Gut Microbiota and Metabolome

2019 ◽  
Vol 26 (19) ◽  
pp. 3567-3583 ◽  
Author(s):  
Maria De Angelis ◽  
Gabriella Garruti ◽  
Fabio Minervini ◽  
Leonilde Bonfrate ◽  
Piero Portincasa ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Human Health ◽  
Dietary Habits ◽  
Short Chain Fatty Acids ◽  
Human Organism ◽  
Immune Functions ◽  
Intestinal Microbes ◽  
Dietary Components ◽  
Dietary Treatments ◽  
The Relationship

Gut microbiota, the largest symbiont community hosted in human organism, is emerging as a pivotal player in the relationship between dietary habits and health. Oral and, especially, intestinal microbes metabolize dietary components, affecting human health by producing harmful or beneficial metabolites, which are involved in the incidence and progression of several intestinal related and non-related diseases. Habitual diet (Western, Agrarian and Mediterranean omnivore diets, vegetarian, vegan and gluten-free diets) drives the composition of the gut microbiota and metabolome. Within the dietary components, polymers (mainly fibers, proteins, fat and polyphenols) that are not hydrolyzed by human enzymes seem to be the main leads of the metabolic pathways of gut microbiota, which in turn directly influence the human metabolome. Specific relationships between diet and microbes, microbes and metabolites, microbes and immune functions and microbes and/or their metabolites and some human diseases are being established. Dietary treatments with fibers are the most effective to benefit the metabolome profile, by improving the synthesis of short chain fatty acids and decreasing the level of molecules, such as p-cresyl sulfate, indoxyl sulfate and trimethylamine N-oxide, involved in disease state. Based on the axis diet-microbiota-health, this review aims at describing the most recent knowledge oriented towards a profitable use of diet to provide benefits to human health, both directly and indirectly, through the activity of gut microbiota.

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