Editing Leaky gut
Warning: You are not logged in. Your IP address will be publicly visible if you make any edits. If you log in or create an account, your edits will be attributed to your username, along with other benefits.
The edit can be undone.
Please check the comparison below to verify that this is what you want to do, and then save the changes below to finish undoing the edit.
Latest revision | Your text | ||
Line 3: | Line 3: | ||
"Emerging evidence has demonstrated that intestinal homeostasis and the microbiome play essential roles in neurological diseases, such as Parkinson's disease. ... We examined the gut of an ALS mouse model, G93A, which expresses mutant superoxide dismutase (SOD1(G93A)), and discovered a '''damaged tight junction structure and increased permeability with a significant reduction in the expression levels of tight junction protein ZO-1 and the adherens junction protein E-cadherin'''. Furthermore, our data demonstrated '''increased numbers of abnormal Paneth cells''' in the intestine of G93A mice. Paneth cells are specialized intestinal epithelial cells that can sense microbes and secrete antimicrobial peptides, thus playing key roles in host innate immune responses and shaping the gut microbiome. A '''decreased level of the antimicrobial peptides defensin 5 alpha''' was indeed found in the ALS intestine. These changes were associated with a '''shifted profile of the intestinal microbiome, including reduced levels of Butyrivibrio Fibrisolvens, Escherichia coli, and Fermicus''', in G93A mice. '''The relative abundance of bacteria was shifted in G93A mice compared to wild-type''' mice. Principal coordinate analysis indicated a difference in fecal microbial communities between ALS and wild-type mice. Taken together, our study '''suggests a potential novel role of the intestinal epithelium and microbiome in the progression of ALS.'''{{#pmid: 25847918|Wu2015}} | "Emerging evidence has demonstrated that intestinal homeostasis and the microbiome play essential roles in neurological diseases, such as Parkinson's disease. ... We examined the gut of an ALS mouse model, G93A, which expresses mutant superoxide dismutase (SOD1(G93A)), and discovered a '''damaged tight junction structure and increased permeability with a significant reduction in the expression levels of tight junction protein ZO-1 and the adherens junction protein E-cadherin'''. Furthermore, our data demonstrated '''increased numbers of abnormal Paneth cells''' in the intestine of G93A mice. Paneth cells are specialized intestinal epithelial cells that can sense microbes and secrete antimicrobial peptides, thus playing key roles in host innate immune responses and shaping the gut microbiome. A '''decreased level of the antimicrobial peptides defensin 5 alpha''' was indeed found in the ALS intestine. These changes were associated with a '''shifted profile of the intestinal microbiome, including reduced levels of Butyrivibrio Fibrisolvens, Escherichia coli, and Fermicus''', in G93A mice. '''The relative abundance of bacteria was shifted in G93A mice compared to wild-type''' mice. Principal coordinate analysis indicated a difference in fecal microbial communities between ALS and wild-type mice. Taken together, our study '''suggests a potential novel role of the intestinal epithelium and microbiome in the progression of ALS.'''{{#pmid: 25847918|Wu2015}} | ||
− | |||
− | |||
− | |||
==References== | ==References== | ||
[[Category:Key concepts]] | [[Category:Key concepts]] |