scholarly journals Glucocorticoids and the Intestinal Environment

Author(s):  
Humeyra Unsal ◽  
Muharrem Balkay
Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 231-LB
Author(s):  
RYOTARO BOUCHI ◽  
TATSUYA FUKUDA ◽  
TAKATO TAKEUCHI ◽  
KIKUKO AMO-SHIINOKI ◽  
KATSUYA TANABE ◽  
...  

1997 ◽  
Vol 16 (2) ◽  
pp. 53-58 ◽  
Author(s):  
Tomohiro OGATA ◽  
Teiichi NAKAMURA ◽  
Katsue ANJITSU ◽  
Tomoko YAESHIMA ◽  
Sachiko TAKAHASHI ◽  
...  

2020 ◽  
Author(s):  
Yumiko Nakanishi ◽  
Ryouko Nozu ◽  
Masami Ueno ◽  
Kyoji Hioki ◽  
Chiharu Ishii ◽  
...  

Abstract Background: Aging is a progressive decline of cellular functions that ultimately affects whole-body homeostasis. Alterations in the gut microbiota associated with aging have been reported, however the molecular basis of the relationships between host aging and the gut microbiota is poorly understood.Result: By using longitudinal microbiome and metabolome characterization, we show that the aging-related alterations in the intestinal environment lead to gut dysbiosis with a potential to induce obesity in mice. In middle-age mice, we observed more than a 2-fold increase in fecal carbohydrates derived from dietary polysaccharides and a significant reduction of gut microbial diversity resembling the microbiota characteristic of obese mice. Consistently, fecal microbiota transplantation from middle-age specific pathogen-free (SPF) mice into young germ-free (GF) mice resulted in increased weight gain and impaired glucose tolerance.Conclusion: Our findings provide new insights into the relationships between host aging and gut dysbiosis and may contribute to the development of a possible solution to aging-related obesity.


2018 ◽  
Author(s):  
Emily C. Woods ◽  
Adrianne N. Edwards ◽  
Shonna M. McBride

ABSTRACTTo cause disease,Clostridioides(Clostridium)difficilemust resist killing by innate immune effectors in the intestine, including the host antimicrobial peptide, cathelicidin (LL-37). The mechanisms that enableC. difficileto adapt to the intestine in the presence of antimicrobial peptides are unknown. Expression analyses revealed an operon,CD630_16170-CD630_16190(clnRAB), which is highly induced by LL-37 and is not expressed in response to other cell-surface active antimicrobials. This operon encodes a predicted transcriptional regulator (clnR) and an ABC transporter system (clnAB), all of which are required for function. Analyses of aclnRmutant indicate that ClnR is a pleiotropic regulator that directly binds to LL-37 and controls expression of numerous genes, including many involved in metabolism, cellular transport, signaling, gene regulation, and pathogenesis. The data suggest that ClnRAB is a novel regulatory mechanism that senses LL-37 as a host signal and regulates gene expression to adapt to the host intestinal environment during infection.Author SummaryC. difficileis a major nosocomial pathogen that causes severe diarrheal disease. ThoughC. difficileis known to inhabit the human gastrointestinal tract, the mechanisms that allow this pathogen to adapt to the intestine and survive host defenses are not known. In this work, we investigated the response ofC. difficileto the host defense peptide, LL-37, to determine the mechanisms underlying host adaptation and survival. Expression analyses revealed a previously unknown locus, which we namedclnRAB, that is highly induced by LL-37 and acts as a global regulator of gene expression inC. difficile. Mutant analyses indicate that ClnRAB is a novel regulatory system that senses LL-37 as a host signal to regulate adaptation to the intestinal environment.


2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Shanshan Chen ◽  
Chi Zhang ◽  
Beihui He ◽  
Ruonan He ◽  
Li Xu ◽  
...  

lncRNA is a transcript that is more than 200 bp in length. Currently, evidence has shown that lncRNA is of great significance in cell activity, involved in epigenetics, gene transcription, chromatin regulation, etc. The existence of an intestinal mucosal mechanical barrier hinders the invasion of pathogenic bacteria and toxins, maintaining the stability of the intestinal environment. Serious destruction or dysfunction of the mechanical barrier often leads to intestinal diseases. This review first summarizes the ability of lncRNAs to regulate the intestinal mucosal mechanical barrier. We then discussed how lncRNAs participate in various intestinal diseases by regulating the intestinal mucosal mechanical barrier. Finally, we envision its potential as a new marker for diagnosing and treating intestinal inflammatory diseases.


1993 ◽  
Vol 46 (2) ◽  
pp. 117-122 ◽  
Author(s):  
Jun KASHIMURA ◽  
Takashi HARA ◽  
Yoshikazu NAKAJIMA

Sign in / Sign up

Export Citation Format

Share Document