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Large study identifies exact gut bacteria involved in Crohn's disease

anciendaze

Senior Member
Messages
1,841
Just a comment, I made a bet with myself when I saw the first post that it would show an increase in fusobacteria. These species have been implicated in possible etiology of colorectal cancers. They are known to form biofilms with other harmful species.

Has anyone else noticed a similar association with other culprits named in association with Crohn's disease?

Next question: how do we tell consequences of immune dysfunction from original causes?

We may be able to interrupt pathology without knowing, but it would be very nice to know how this came about.
 

Ecoclimber

Senior Member
Messages
1,011
Also, to add this research listing to the thread topic:

Neurochem Res. 2014 Mar 4. [Epub ahead of print]
Chronic Functional Bowel Syndrome Enhances Gut-Brain Axis Dysfunction, Neuroinflammation, Cognitive Impairment, and Vulnerability to Dementia.
Daulatzai MA.
Author information
Abstract

The irritable bowel syndrome (IBS) is a common chronic functional gastrointestinal disorder world wide that lasts for decades.
The human gut harbors a diverse population of microbial organisms which is symbiotic and important for well being. However, studies on conventional, germ-free, and obese animals have shown that alteration in normal commensal gut microbiota and an increase in pathogenic microbiota-termed "dysbiosis", impact gut function, homeostasis, and health.

Diarrhea, constipation, visceral hypersensitivity, and abdominal pain arise in IBS from the gut-induced dysfunctional metabolic, immune, and neuro-immune communication. Dysbiosis in IBS is associated with gut inflammation. Gut-related inflammation is pivotal in promoting endotoxemia, systemic inflammation, and neuroinflammation.

A significant proportion of IBS patients chronically consume alcohol, non-steroidal anti-inflammatories, and fatty diet; they may also suffer from co-morbid respiratory, neuromuscular, psychological, sleep, and neurological disorders. The above pathophysiological substrate is underpinned by dysbiosis, and dysfunctional bidirectional "Gut-Brain Axis" pathways.

Pathogenic gut microbiota-related systemic inflammation (due to increased lipopolysaccharide and pro-inflammatory cytokines, and barrier dysfunction), may trigger neuroinflammation enhancing dysfunctional brain regions including hippocampus and cerebellum.

These as well as dysfunctional vago-vagal gut-brain axis may promote cognitive impairment. Indeed, inflammation is characteristic of a broad spectrum of neurodegenerative diseases that manifest demntia. It is argued that an awareness of pathophysiological impact of IBS and implementation of appropriate therapeutic measures may prevent cognitive impairment and minimize vulnerability to dementia.

PMID:
24590859
[PubMed - as supplied by publisher]