Dysbiosis – What Have We Learned?
The human body has some 10 trillion human cells—but 10 times that number of microbial cells. So what happens when such an important part of our bodies goes missing or never develops?
Plus what can we do to limit any adverse consequences linked to microbial disruption – referred to as dysbiosis?
Further, do probiotics—dietary supplements containing potentially beneficial microbes actually support appropriate immune responses?
Not only do gut bacteria help protect against other disease-causing bacteria that might come from your food and water, they represent another arm of the immune system.
What have we learnt in just the last few months about how we – humans and bacteria live and function together is starting to have a powerful impact in the way health care and disease management are being considered. The growing understanding of the role of our gastrointestinal bacteria in terms of health, and disease, through increasingly sophisticated analysis of genetics and bioinformatics is producing remarkable and novel insights. Many of these comfortably fit the nutritional and naturopathic ideologies we have been trained to embrace. The concept that the gut and its inhabitants may provide a key to health and disease is being taken ever more seriously by the scientific and clinical community.
Long suspected but mostly denied or pushed aside has been the view that even a single course of antibiotics may change the composition of our internal bacterial companions for months after the therapy. This is not just being recognised as a real event,, but also it is understood how this can make an individual prone to intercurrent bacterial infections. In much the same way, infections of the gastrointestinal tract can also have a profound effect on the composition of the commensal organisms, both events of which can lead to a problem called dysbiosis. This condition may manifest in a variety of ways that compromises the local tissues and remote tissues, through a number of inflammatory proteins, molecular mimicry and parainflammation. The appropriate use of strain specific probiotics has shown success in the resolution of this complaint.
There is an increasing weight of evidence that points to long-term chronic consequences of acute gastro intestinal infectious insults, including the development of a surprisingly common post infectious irritable bowel syndrome (IBS)and inflammatory bowel diseases (IBD).
An estimated 1400 human pathogens have been identified of which a remarkable 50% are zoonotic (a disease that can be transmitted from animals to people or, more specifically, a disease that normally exists in animals but that can infect humans) in origin, arising from coming into contact with creatures such as bats, ruminants (cows) and birds. A number approximating 177 are currently classified as emerging or re-emerging pathogens, but it is quite likely his number is too conservative. In the main this is due to the complications linked to sample collection. A wide range of variables can affect the quality and accuracy of the sample contents, including timing of collection, the use of natural and pharmacological anti microbials or other growth inhibiting compounds, culture medium used and atmospheric conditions.
More importantly it is not yet possible to culture successfully all of the organisms that reside in the wet tissues of the body, and whilst sophisticated molecular techniques are available to the research centre – these are not yet available to normal pathology laboratories.,
How do pro/pre-biotics fix dysbiosis?
Probiotic supplements may have a unique action of repair in dysbiosis by altering signalling mechanisms that have become disrupted due to the dysbiosis. A well understood proinflammatory cytokine called interferon gamma once activated switches on NF-κB (nuclear factor-kappa B) and in doing so activates over 500 genes used in the normal inflammatory defence process. Some probiotics (L. Helveticus) are able to stop this process, albeit they work better prophylactically rather than reactively at present. Others (LGG) are better at restoring gut barrier function and so reducing translocation of inflammatory cells across the mucosal wall.
As a result, beneficial microbes should now be considered for further evaluation as a potential agent restoration of dysbiosis and become part of an integrated strategy to correct local and systemic health issues connected to loss of function in the gastrointestinal tract.
Probiotics could well have a protective role in this clinical setting by acting to alter enteric neural and muscular dysfunction and the low-grade inflammatory responses that appear to mediate chronic IBS-related symptoms after an acute intercurrent bacterial infection often following exposure to a pathogen or post antibiotic therapy.
Constituents of the commensal intestinal microbiota and exogenous agents, such as probiotics and prebiotics (defined as nondigestible oligosaccharides used as substrate in the colon by resident Bifidiobacteria and lactic acid-producing organisms), can both serve to restore gut homeostasis.
A special type of probiotic bacteria found in food called Propionibacterium freudenreichii (PF), can simultaneously function as a prebiotic. They reproduce in the lower gut and generate prophylactic short-chain fatty acids (SCFA), including propionate and acetate. These SCFA lower the pH, protect the intestinal lining, down-regulate NF-κB (nuclear factor-kappa B), and support absorption of calcium, magnesium and potassium.
Probiotics and selected prebiotics are gaining increasing attention as a novel approach to prevent intercurrent infections and dysbiosis and reduce both local and regional illness driven by loss of bacterial tolerance in the gastrointestinal tract.
 Sartor, R. (2008). Therapeutic correction of bacterial dysbiosis discovered by molecular techniques Proceedings of the National Academy of Sciences, 105 (43), 16413-16414 DOI: 10.1073/pnas.0809363105
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 Crosswell A, Amir E, Teggatz P, et al. Prolonged impact of antibiotics on intestinal microbial ecology and susceptibility to enteric Salmonella infection. Infect Immun 2009; 77:2741–2753.View Abstract
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