Role of Dietary Polyphenols and Inflammatory Processes on Disease Progression Mediated by the Gut Microbiota

2013 ◽  
Vol 16 (5) ◽  
pp. 435-437 ◽  
Author(s):  
J. Alfredo Martínez ◽  
Usune Etxeberría ◽  
Alicia Galar ◽  
Fermín I. Milagro
Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 169
Author(s):  
María Callejo ◽  
Joan Albert Barberá ◽  
Juan Duarte ◽  
Francisco Perez-Vizcaino

Pulmonary arterial hypertension (PAH) is characterized by sustained vasoconstriction, vascular remodeling, inflammation, and in situ thrombosis. Although there have been important advances in the knowledge of the pathophysiology of PAH, it remains a debilitating, limiting, and rapidly progressive disease. Vitamin D and iron deficiency are worldwide health problems of pandemic proportions. Notably, these nutritional alterations are largely more prevalent in PAH patients than in the general population and there are several pieces of evidence suggesting that they may trigger or aggravate disease progression. There are also several case reports associating scurvy, due to severe vitamin C deficiency, with PAH. Flavonoids such as quercetin, isoflavonoids such as genistein, and other dietary polyphenols including resveratrol slow the progression of the disease in animal models of PAH. Finally, the role of the gut microbiota and its interplay with the diet, host immune system, and energy metabolism is emerging in multiple cardiovascular diseases. The alteration of the gut microbiota has also been reported in animal models of PAH. It is thus possible that in the near future interventions targeting the nutritional status and the gut dysbiosis will improve the outcome of these patients.


Immuno ◽  
2021 ◽  
Vol 1 (4) ◽  
pp. 583-594
Author(s):  
Takehiro Hirano ◽  
Hiroshi Nakase

The gut microbiota has diverse microbial components, including bacteria, viruses, and fungi. The interaction between gut microbiome components and immune responses has been studied extensively over the last decade. Several studies have reported the potential role of the gut microbiome in maintaining gut homeostasis and the development of disease. The commensal microbiome can preserve the integrity of the mucosal barrier by acting on the host immune system. Contrastingly, dysbiosis-induced inflammation can lead to the initiation and progression of several diseases through inflammatory processes and oxidative stress. In this review, we describe the multifaceted effects of the gut microbiota on several diseases from the perspective of mucosal immunological responses.


2020 ◽  
Vol 21 ◽  
Author(s):  
Tingting Zhao ◽  
Zhe Wang ◽  
Zhilong Liu ◽  
Youhua Xu

: With the recognition of the important role of gut microbiota in both health and disease progression, attempts to modulate its composition as well as its co-metabolism with the organism have attracted special attention. Abundant studies have demonstrated that dysfunction or imbalance of gut microbiota is closely with disease including endocrine diseases, neurodegenerative diseases, tumors, cardiovascular diseases, et al. Herbal medicines have been applied for preventing and treating disease worldwide for hundreds of years. Although the underlying mechanism seems to be complex, one of the important one is through modulating gut microbiota. In this review, co-metabolism between herbal medicines and microbiota, as well as the potential pathways are summarized from most recent published papers.


2021 ◽  
Vol 142 ◽  
pp. 110189
Author(s):  
S. Mithul Aravind ◽  
Santad Wichienchot ◽  
Rong Tsao ◽  
S. Ramakrishnan ◽  
S. Chakkaravarthi

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 982 ◽  
Author(s):  
Mireille Koudoufio ◽  
Yves Desjardins ◽  
Francis Feldman ◽  
Schohraya Spahis ◽  
Edgard Delvin ◽  
...  

Lifestyle factors, especially diet and nutrition, are currently regarded as essential avenues to decrease modern-day cardiometabolic disorders (CMD), including obesity, metabolic syndrome, type 2 diabetes, and atherosclerosis. Many groups around the world attribute these trends, at least partially, to bioactive plant polyphenols given their anti-oxidant and anti-inflammatory actions. In fact, polyphenols can prevent or reverse the progression of disease processes through many distinct mechanisms. In particular, the crosstalk between polyphenols and gut microbiota, recently unveiled thanks to DNA-based tools and next generation sequencing, unravelled the central regulatory role of dietary polyphenols and their intestinal micro-ecology metabolites on the host energy metabolism and related illnesses. The objectives of this review are to: (1) provide an understanding of classification, structure, and bioavailability of dietary polyphenols; (2) underline their metabolism by gut microbiota; (3) highlight their prebiotic effects on microflora; (4) discuss the multifaceted roles of their metabolites in CMD while shedding light on the mechanisms of action; and (5) underscore their ability to initiate host epigenetic regulation. In sum, the review clearly documents whether dietary polyphenols and micro-ecology favorably interact to promote multiple physiological functions on human organism.


Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1389
Author(s):  
Sonia Croci ◽  
Lina Ilaras D’Apolito ◽  
Valeria Gasperi ◽  
Maria Valeria Catani ◽  
Isabella Savini

Metabolic syndrome (MetS) is a complex pathophysiological state with incidence similar to that of a global epidemic and represents a risk factor for the onset of chronic non-communicable degenerative diseases (NCDDs), including cardiovascular disease (CVD), type 2 diabetes mellitus, chronic kidney disease, and some types of cancer. A plethora of literature data suggest the potential role of gut microbiota in interfering with the host metabolism, thus influencing several MetS risk factors. Perturbation of the gut microbiota’s composition and activity, a condition known as dysbiosis, is involved in the etiopathogenesis of multiple chronic diseases. Recent studies have shown that some micro-organism-derived metabolites (including trimethylamine N-oxide (TMAO), lipopolysaccharide (LPS) of Gram-negative bacteria, indoxyl sulfate and p-cresol sulfate) induce subclinical inflammatory processes involved in MetS. Gut microbiota’s taxonomic species or abundance are modified by many factors, including diet, lifestyle and medications. The main purpose of this review is to highlight the correlation between different dietary strategies and changes in gut microbiota metabolites. We mainly focus on the validity/inadequacy of specific dietary patterns to reduce inflammatory processes, including leaky gut and subsequent endotoxemia. We also describe the chance of probiotic supplementation to interact with the immune system and limit negative consequences associated with MetS.


Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1370
Author(s):  
Umair Shabbir ◽  
Akanksha Tyagi ◽  
Fazle Elahi ◽  
Simon Okomo Aloo ◽  
Deog-Hwan Oh

Gut microbiota (GM) play a role in the metabolic health, gut eubiosis, nutrition, and physiology of humans. They are also involved in the regulation of inflammation, oxidative stress, immune responses, central and peripheral neurotransmission. Aging and unhealthy dietary patterns, along with oxidative and inflammatory responses due to gut dysbiosis, can lead to the pathogenesis of neurodegenerative diseases, especially Alzheimer’s disease (AD). Although the exact mechanism between AD and GM dysbiosis is still unknown, recent studies claim that secretions from the gut can enhance hallmarks of AD by disturbing the intestinal permeability and blood–brain barrier via the microbiota–gut–brain axis. Dietary polyphenols are the secondary metabolites of plants that possess anti-oxidative and anti-inflammatory properties and can ameliorate gut dysbiosis by enhancing the abundance of beneficial bacteria. Thus, modulation of gut by polyphenols can prevent and treat AD and other neurodegenerative diseases. This review summarizes the role of oxidative stress, inflammation, and GM in AD. Further, it provides an overview on the ability of polyphenols to modulate gut dysbiosis, oxidative stress, and inflammation against AD.


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