Human Microbiome and Gut Disease
Microbial dysbiosis links microbial diversity to disease. Most gut microbes in the gut are beneficial or harmless. These microbes are in balance in healthy people – called homeostasis.
In sick and chronic disease the gut harbours more harmful microbes (pathogens) than beneficial.
Therefore the balance shifts and homeostasis is no longer maintained in the gut. This provokes changed in the immune system and causes inflammation
Some acute GI diseases such as E. coli, Cholera, C. difficile produce dramatic changes in the gut to resemble the skin microbiota.
Inflammatory bowel disease, Chron’s Disease and colon rectal cancer all exhibit dysbiosis.
Disease causes a decrease in the diversity of bacteria. A healthy person has many more different types of microbes in the gut. Diversity is very important
Inflammatory Bowel Disease is when parts of the small intestine or colon are chronically inflamed i.e. in Chron’s Disease or Ulcerative Colitis. Microbes in people with these conditions are different from each other and from healthy people.
Microbial dysbiosis is more evident in people with inflammatory bowel disease
Healthy people have a higher diversity including higher Firmicutes and Bacteroidetes. Microbes in people with Chron’s Disease and Ulcerative Colitis have genes that carry out functions related to infection. In children with Chron’s, the use of antibiotics lead to more extreme dysbiosis.
There is increasing evidence that many cancers are linked to microbial agents. Fusobacterium nucleatum is an anaerobe that thrives in environments with little or no oxygen. It is present in low amounts in a healthy colon but found in high abundance in colonic tumours. It is also in the mouth of carnivorous animals. It homes in on the tumour environment. Is this cause or effect?
We can induce the formation and growth of cancerous legions by interacting with human cells in the colon.
Leptotrichia and Campylobacter also co-occur with Fusobacterium nucleatum and form a signature of aerobic bacteria associated with tumours in the colon.
When the balance is tipped, this may lead to disease
We must also study which microbes we have lost. For instance, Oxalobacter formigenes eats oxalate which is an end product of human metabolism, and may help protect against kidney stones. There is a higher prevalence of Oxalobacter formigenes in the Hadza tribe.
If we have we altered our microbiome in western cultures due to antibiotics, diet and hygiene practices, the next step is to find out how to replenish our microbiome. We can liken the care of our microbiome to that of soil.
For instance, with regards to C-section births, there may be interventions that may help (such as the use of gauze inserts to transfer the mother’s microbes to baby).
With antibiotics, faecal transplants may be required.
Faecal transplants are very successful at treating C Difficile infections. 15 out of 16 people are cured with a transplant whereas 3 out of 13 and 4 out of 14 are cured with antibiotics.
We need to harness the power of microbes
Bacteria have been competing with each other for millions of years and if anything can fight off a C. Difficile infection, it is other bacteria!
Within one day of the transplant, the microbiota is returned to normal. Once this was the last resort but now it is the best method.
We know that diet and disease affects the microbiome. Obese individuals have a unique microbiome signature and that when transferred to lean individuals, they become obese.
Our microbiome also affects the way that we metabolise different drugs and can influence the difference between treatment and toxicity.
Gut disease exhibits a markedly different microbiome with much lower diversity. Changing the microbiome may be a successful way to deal with gut issues, especially in the case of C Difficile and faecal transplants.