A new paradigm for a new simple chemical: butyrate & immune regulation

2021 ◽  
Author(s):  
Guoqi Dang ◽  
Weida Wu ◽  
Hongfu Zhang ◽  
Nadia Everaert

Butyrate has attracted a lot of attention on host immunity. It promotes anti-inflammatory response by interacting with receptors, immune cells and suppressing histone deacetylase activity.

2015 ◽  
Vol 4 (12) ◽  
pp. e53 ◽  
Author(s):  
Manuel Delgado-Vélez ◽  
Carlos A Báez-Pagán ◽  
Yamil Gerena ◽  
Orestes Quesada ◽  
Laura I Santiago-Pérez ◽  
...  

PLoS ONE ◽  
2019 ◽  
Vol 14 (3) ◽  
pp. e0213150 ◽  
Author(s):  
Federica De Santis ◽  
Noemi Poerio ◽  
Angelo Gismondi ◽  
Valentina Nanni ◽  
Gabriele Di Marco ◽  
...  

2020 ◽  
Vol 32 (7) ◽  
pp. 447-454 ◽  
Author(s):  
Koji Hosomi ◽  
Jun Kunisawa

Abstract Immune metabolism has been recognized as a new paradigm in the regulation of host immunity. In the environment, there are many micro-organisms including pathogenic and non-pathogenic and/or beneficial ones. Immune cells exhibit various responses against different types of microbes, which seem to be associated with changes in energy metabolism. In addition, dietary nutrition influences host metabolism and consequent responses by immune cells. In this review, we describe the complex network of immune metabolism from the perspectives of nutrition, micro-organisms and host immunity for the control of immunologic health and diseases.


2017 ◽  
Author(s):  
Benjamin S. Durham ◽  
Ronald Grigg ◽  
Ian C. Wood

AbstractHistone deacetylase (HDAC) inhibitors prevent neural cell death in in vivo models of cerebral ischaemia, brain injury and neurodegenerative disease. One mechanism by which HDAC inhibitors may do this is by suppressing the excessive inflammatory response of chronically activated microglia. However, the molecular mechanisms underlying this anti-inflammatory effect and the specific HDAC responsible are not fully understood. Recent data from in vivo rodent studies has shown that inhibition of class I HDACs suppresses neuroinflammation and is neuroprotective. In our study we have identified that selective HDAC inhibition with inhibitors apicidin, MS-275 or MI-192, or specific knockdown of HDAC1 or 2 using siRNA, suppresses the expression of cytokines interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α) in BV2 murine microglia activated with lipopolysaccharide (LPS). Furthermore, we found that in the absence of HDAC1, HDAC2 is upregulated and these increased levels are compensatory, suggesting these two HDACs have redundancy in regulating the inflammatory response of microglia. Investigating the possible underlying anti-inflammatory mechanisms suggests an increase in protein expression is not important. Taken together, this study supports the idea that inhibitors selective towards HDAC1 or HDAC2, may be therapeutically useful for targeting neuroinflammation in brain injuries and neurodegenerative disease.Significance StatementThe number of patients suffering a stroke or a neurodegenerative disease, such as Alzheimer’s is increasing These conditions are severely debilitating and are leading causes of mortality, with neural cell death and loss of brain tissue being a major feature. A number of mechanisms contribute to neuronal death, including inflammation in the brain, but we still lack clinical therapies to inhibit this. The work presented here provides further insight into potential molecular therapeutic targets called histone deacetylases (HDACs), which are thought to contribute to neural cell death by promoting inflammation. We show that down regulation of HDAC1 and 2 is sufficient to reduce this inflammatory response. Our findings have clinical relevance because they identify HDAC1 and 2 as promising targets for therapy.


2009 ◽  
Vol 101 (01) ◽  
pp. 36-47 ◽  
Author(s):  
Jean-Marc Cavaillon ◽  
Minou Adib-Conquy

SummaryThe concept of ‘Compensatory anti-inflammatory response syndrome’ (CARS) was proposed in 1997 by Roger Bone (1941–1997) to qualify the consequences of the counter-regulatory mechanisms initiated to limit the overzealous inflammatory process in patients with infectious (sepsis) or non-infectious systemic inflammatory response syndrome (SIRS). One major consequence of CARS is the modification of the immune status that could favour the enhanced susceptibility of intensive care patients to nosocomial infections. Indeed, most animal ‘two-hit’ models illustrate an enhanced sensitivity to infection after a first insult. However, this observation is highly dependent on the experimental procedure. Numerous functions of circulating leukocytes are altered in sepsis and SIRS patients, as well as in animal models of sepsis or SIRS. However, this is rather a reprogramming of circulating leukocytes, since there is not a global defect of the immune cells functions. Furthermore, within tissues, leukocytes are rather primed or activated than immunosuppressed. Thus, CARS may be considered as an adapted compartmentalized response with the aim to silence some acute proinflammatory genes, and to maintain the possible expression of certain genes involved in the anti-infectious process.


Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 1021
Author(s):  
Rosaria Varì ◽  
Beatrice Scazzocchio ◽  
Annalisa Silenzi ◽  
Claudio Giovannini ◽  
Roberta Masella

Curcumin is a lipophilic polyphenol, isolated from the plant turmeric of Curcuma longa. Curcuma longa has always been used in traditional medicine in Asian countries because it is believed to have numerous health benefits. Nowadays it is widely used as spice component and in emerging nutraceutical food worldwide. Numerous studies have shown that curcumin possesses, among others, potential anti-inflammatory properties. Obesity represents a main risk factor for several chronic diseases, including type 2 diabetes, cardiovascular disease, and some types of cancer. The establishment of a low-grade chronic inflammation, both systemically and locally in adipose tissue, occurring in obesity most likely represents a main factor in the pathogenesis of chronic diseases. The molecular mechanisms responsible for the onset of the obesity-associated inflammation are different from those involved in the classic inflammatory response caused by infections and involves different signaling pathways. The inflammatory process in obese people is triggered by an inadequate intake of nutrients that produces quantitative and qualitative alterations of adipose tissue lipid content, as well as of various molecules that act as endogenous ligands to activate immune cells. In particular, dysfunctional adipocytes secrete inflammatory cytokines and chemokines, the adipocytokines, able to recruit immune cells into adipose tissue, amplifying the inflammatory response also at systemic level. This review summarizes the most recent studies focused at elucidating the molecular targets of curcumin activity responsible for its anti-inflammatory properties in obesity-associated inflammation and related pathologies.


2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Anup K. Talukder ◽  
Mohammad B. Rashid ◽  
Mohamed S. Yousef ◽  
Kazuya Kusama ◽  
Takashi Shimizu ◽  
...  

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