Mammals, including humans, are born with no bacteria in their intestines. Upon birth, bacteria are soon introduced from the mother and the external environment. Eventually, the intestine contains many millions of bacteria in a relationship which is mutually beneficial to the mammal and to the bacteria.
The gut bacteria alter development and functioning of the intestinal wall and the mammal genome alters the amount of bacteria and the immune response to the bacteria. The balance of the whole system is termed the microbiome.
The number of species of bacteria in the microbiome may be as high as 35,000 in RNA studies. The “Human Microbiome Project” has been started by the U.S. National Institute of Health (NIH) to study the between human disease and the microbiome. Mice are born in a germ-free environment in the laboratory and specific bacteria are added to see the effects on their systems.
Bacteroides fragilis bacteria were found to be adequate to develop normal gut lymphoid tissue, spleen, thymus and a balanced immune system in mice. Antibiotics are being used in similar studies.
The innate immune system initiates the inflammatory response. Antigen presenting cells (APCs,) such as macrophages, monocytes, B cells and dendritic cells are involved. They are activated by microbial toxins. The antigen is presented to T cells and the T cells are activated. Altered responses have been found in multiple sclerosis (MS,) Crohn’s diease, ulcerative colitis and asthma.
The U.S. Food and Drug Administration (FDA) has approved several drugs for the treatment of MS which work by blocking the migration of inflammatory cells into the nervous system. Gut bacteria seem to play a role in this migration.
Microbiome changes have been associated with autism. The feces of autistic children contain more Clostridium spp. than normally seen. Autism is associated with antibiotic use.
Guillain-Barre syndrome has been associated with Campylobacter jejuni infection. The illness is caused by an autoimmune reaction to the antibodies formed to C. jejuni. Other infections can precede the syndrome.
There is no epidemiologic evidence that demyelinating disease is related to the microbiome. In experimental MS, called EAE (experimental autoimmune encephalomyelitis,) manipulation of the microbiome can alter the course of the disease in mice. EAE is an animal model of human MS. Studies are being done to see which bacteria improve the MS and which bacteria accentuate the disease.
CONCLUSION: Studies of the human intestinal microbiome may lead to a new therapeutic approach to multiple sclerosis. It is possible that immunization from diseases of the CNS may be obtained with oral doses of certain bacteria and treatment of CNS diseases may be possible by treatment with other gut bacteria.