The Human Microbiology Institute is delighted to introduce our new theory of “Microbiota Diseases”. The term “Microbiota Diseases” reflects the primary and crucial role of microbiota-related disorders in certain host organism pathologies.
Causative agents that can lead to the development of Microbiota Diseases include bacteriophages that solely target the microbiota.
HMI research indicates that Microbiota Diseases lead to pathologies in the macroorganism, including increased intestinal permeability and leaky gut- associated pathologies.
Intestinal barrier dysfunction or disruption of the intestinal barrier, known as “leaky gut” syndrome, is characterized by increased transcellular permeability or increased permeability of the tight junctions to macromolecules. This abnormally permeable mucosal barrier is associated with various disease pathologies, including:
- Inflammatory bowel disease
- Crohn’s disease
- Alzheimer’s disease
- Amyotrophic lateral diseases
- Parkinson’s disease
- Type 1 diabetes
- Cardiovascular disorders
- Rheumatoid arthiritis
- Liver and kidney failure
Thus, “Microbiota Diseases” associated with leaky gut might be contagious. If true, this finding implies that other human diseases associated with Microbiota Diseases, including but not limited to those triggered and/or promoted by leaky intestines, may also be contagious and could be contracted via environmental or community exposure to certain bacteriophages.
BREAKTHROUGH HIGHLIGHTS OF MICROBIOTA DISEASES
- MICROBIOTA DISEASES – new causes of diseases that were previously not considered contagious (neurodegenerative diseases, schizophrenia, autism, and cancers)
- MICROBIOTA DISEASES – might comprise a new group of human diseases
- MICROBIOTA DISEASES – comprise novel therapeutic targets.
- MICROBIOTA DISEASES – lead to increased intestinal permeability
We try to make our data available to the whole scientific community. The HMI welcomes collaborative studies to unravel the pathogenesis of human diseases associated with the microbiota. However, we ask that you respect the rights of first publication and cite our work as follows: