scholarly journals Response to Comment on Alkanani et al. Alterations in Intestinal Microbiota Correlate With Susceptibility to Type 1 Diabetes. Diabetes 2015;64:3510–3520

Diabetes ◽  
2015 ◽  
Vol 64 (10) ◽  
pp. e41-e41 ◽  
Author(s):  
Brandie D. Wagner ◽  
Daniel N. Frank ◽  
Danny Zipris
2013 ◽  
Vol 146 (2) ◽  
pp. 112-119 ◽  
Author(s):  
Naoko Hara ◽  
Aimon K. Alkanani ◽  
Diana Ir ◽  
Charles E. Robertson ◽  
Brandie D. Wagner ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2189 ◽  
Author(s):  
Jakub Żółkiewicz ◽  
Aleksandra Marzec ◽  
Marek Ruszczyński ◽  
Wojciech Feleszko

As an imbalance in the intestinal microbiota can lead to the development of several diseases (e.g., type 1 diabetes, cancer, among others), the use of prebiotics, probiotics, and postbiotics to alter the gut microbiome has attracted recent interest. Postbiotics include any substance released by or produced through the metabolic activity of the microorganism, which exerts a beneficial effect on the host, directly or indirectly. As postbiotics do not contain live microorganisms, the risks associated with their intake are minimized. Here, we provided a critical review of postbiotics described in the literature, including their mechanisms of action, clinical characteristics, and potential therapeutic applications. We detailed the pleiotropic effects of postbiotics, including their immunomodulatory, anti-inflammatory, antioxidant, and anti-cancer properties. Although the use of postbiotics is an attractive strategy for altering the microbiome, further study into its efficacy and safety is warranted.


Diabetes ◽  
2015 ◽  
Vol 64 (10) ◽  
pp. 3510-3520 ◽  
Author(s):  
Aimon K. Alkanani ◽  
Naoko Hara ◽  
Peter A. Gottlieb ◽  
Diana Ir ◽  
Charles E. Robertson ◽  
...  

2017 ◽  
Vol 114 (36) ◽  
pp. 9671-9676 ◽  
Author(s):  
Michael Silverman ◽  
Lindsay Kua ◽  
Alessandro Tanca ◽  
Mauro Pala ◽  
Antonio Palomba ◽  
...  

Certain MHC-II or HLA-D alleles dominantly protect from particular autoimmune diseases. For example, expression of the MHC-II Eα:Eβ complex potently protects nonobese diabetic (NOD) mice, which normally lack this isotype, from spontaneous development of type 1 diabetes. However, the underlying mechanisms remain debated. We investigated MHC-II–mediated protection from type 1 diabetes using a previously reported NOD mouse line expressing an Eα transgene and, thereby, the Eα:Eβ complex. Eα16/NOD females vertically protected their NOD offspring from diabetes and insulitis, an effect that was dependent on the intestinal microbiota; moreover, they developed autoimmunity when treated with certain antibiotics or raised in a germ-free environment. Genomic and proteomic analyses revealed NOD and Eα16/NOD mice to host mild but significant differences in the intestinal microbiotas during a critical early window of ontogeny, and transfer of cecal contents from the latter to the former suppressed insulitis. Thus, protection from autoimmunity afforded by particular MHC/HLA alleles can operate via intestinal microbes, highlighting potentially important societal implications of treating infants, or even just their pregnant mothers, with antibiotics.


2009 ◽  
Vol 137 (1) ◽  
pp. 381-383 ◽  
Author(s):  
Rodrigue Dessein ◽  
Laurent Peyrin-Biroulet ◽  
Mathias Chamaillard

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