Bacteria may take responsibility for more than we think. Particularly regarding inflammatory diseases like type 2 diabetes.
Professor Douglas Kell from Manchester University and professor Resia Pretorius from SU, i.e., Stellenbosch University in South Africa both conducted a number of studies.
These studies are actually making a drastic change. The change is in the way the scientists perceive the effect bacteria have on many diseases. Diseases such as T2D, i.e. type 2 diabetes, Alzheimer’s disease, Rheumatoid Arthritis, Parkinson’s disease, and Sepsis.
Before, Kell and Pretorius have established that the chronic inflammatory diseases above mentioned having a microbial origin as well.
Kell notes that if the bacteria were replicating or active as in the infectious diseases people would have been aware of that fact. However, the microbes are mainly dormant, and they are not replicating.
Moreover, due to their dormant nature, the microbes didn’t manifest under the conditions of a standard microbial test. Therefore, previously bacteria were thought that they are not present in the human blood, believing that the blood is “sterile.”
However, what is typical of inflammatory disease are high levels of iron in our blood. And that can bring the bacteria back to life.
According to previous research under these conditions, what the bacteria does is that it begins secreting and replicating LPS, i.e., lipopolysaccharides which induces increased inflammation.
What Scientists Found
What is common for these chronic diseases is that they constantly have elevated levels of inflammation.
Kell and Pretorius had already found that anomalous amyloidogenic blood clotting, one cause of inflammation is related to and maybe experimentally prompted by bacterial cell wall constituents like LTA, i.e., Lipoteichoic acid and LPS.
These are the cell wall components of Gram-positive and Gram-negative. The coagulopathies which are adverse blood clotting are typical of inflammatory diseases.
The researchers have long found that they can induce amyloid formation, where fibrinogen, i.e., blood clotting proteins have the deformation in structure.
In fact, deformation from a-helixes to flat b-sheet structures, which can potentially induce neurodegeneration and death of cells.
Because of that, in diseased people, the fibrin fibers of the blood clots are different in comparison to those of healthy people. This is the topic of discussion in different publications from the group.
Pretorius explains that these fibers look like a bowl of spaghetti in normal blood clots. However, in diseased individuals, the blood clots look matted with condensed and large fused fibers.
In addition, they can be seen with special stains which fluoresce when there is amyloid present. According to researchers, the changed clot structure is part of all studied inflammatory conditions and that includes type 2 diabetes.
What is the connection between the abnormal formation of a clot, TLA, bacteria, and LPS? Also, are there molecules that can “mop up” LTA or LPS and that are circulating in the blood of the people that have inflammatory diseases?
Recent 2017 Study
Kell and Pretorius, together with Ms. Sthembile Mbotwe MSc student from the University of Pretoria recently published a study. The study was published in the Scientific Reports (Nature publication).
In that 2017 study, they made an investigation on the effect that the LPS-binding protein (LBP) has. In fact, all people produce this protein. What they did is that they put LBP in the blood from T2D patients and after putting LPS in healthy blood.
In the past, they came to the discovery that LPS leads to abnormal clot formation when they add it to healthy blood. Also that LBP can reverse this.
However, in this particular publication, they showed what can LBP do. And that is that it can reverse the clot structure that is adverse in type 2 diabetes blood.
The process got a confirmation by both super-resolution confocal microscopy and scanning electron microscopy.
The conclusion is that bacterial LPS is an important player in the maintenance and development of type 2 diabetes and its disabling sequelae.
Pretorius explains that in the case of inflamed situations LPS in large amounts probably may prevent LBP to work properly.
Conclusion of Researchers
According to researchers now there is considerable new evidence. This evidence is in contrast in comparison to the current strategies to attack type 2 diabetes.
And that the recognition that it has dormant microbes, coagulopathies, and chronic inflammatory processes offer new opportunities regarding treatment.
This discovery is promising, and at least it is one step ahead regarding the treatment.