There is growing evidence that strains of the bacterial complex that causes Lyme disease may also play a role in triggering autoimmune diseases.
Lyme disease is caused by strains of the Borrelia burgdorferi sensu lato complex, such as B. burgdorferi sensu stricto, B. afzelii and B. garinii. There is growing evidence that it may also play a role in triggering autoimmune diseases. This phenomenon is particularly evident in cases where the infection is prolonged or inadequately treated and the body’s immune system shows prolonged, abnormal activation.
One of the most significant mechanisms by which Lyme disease can trigger an autoimmune reaction is molecular mimicry. This immunological process means that the pathogen expresses proteins that are structurally similar to the host’s own proteins.
In addition, Borrelia burgdorferi is also capable of influencing cell membranes. Some studies have shown that the antigens and lipoproteins of the bacterium can modify the fluidity of cell membranes, which alters the efficiency and dynamics of signal transmission between immune cells. This can lead to further distortion of the immune response, increasing the likelihood of autoimmune processes.
Molecular mimicry
Molecular mimicry is an immunological phenomenon in which a pathogen, such as a virus or bacterium, carries proteins, or antigens, whose structure is partially or completely similar to the host organism’s own proteins. This similarity can deceive the immune system: when it launches an attack against foreign antigens, it may also target the body’s own healthy tissues, as it is unable to distinguish them from the pathogen. This mechanism may play an important role in the development of various autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis and type 1 diabetes.
Borrelia burgdorferi, the pathogen that causes Lyme disease, is also capable of molecular mimicry. Several studies have shown that certain Borrelia proteins are structurally similar to human tissue proteins, particularly those found in the joint, nervous and endocrine systems. This similarity may cause the immune system to remain “active” during or after infection and continue to attack the host’s cells even after the pathogen has been eradicated – for example, joint structures or even the insulin-producing beta cells of the pancreas.
An exciting example of this comes from research on type 1 diabetes:
Type 1 diabetes (T1D) is an autoimmune disease whose incidence has increased dramatically in recent decades, especially in Western societies. In this disease, the body’s immune system, mainly CD8+ T cells, attacks and destroys the insulin-producing beta cells of the pancreas. The latest research has identified a new beta cell-specific autoantigen, IGRP (islet-specific glucose-6-phosphatase catalytic subunit-related protein), which is recognised by dominant T cell clones in mice prone to diabetes. The antigen is presented to immune cells via MHC I molecules and activates the beta cell-destroying immune response. Another interesting fact is that mimotope peptides with a structure similar to IGRP, such as those derived from the bacterium Borrelia burgdorferi, may also be able to trigger an immune response through molecular mimicry, potentially linking infection and the development of autoimmunity.
Similarly, Lyme arthritis, which develops during Lyme disease, may not only be the result of the active presence of the infection, but also partly the result of an autoimmune response due to molecular mimicry, especially if the joint inflammation persists despite antibiotic treatment.
Therefore, molecular mimicry may be a key link between infectious diseases and autoimmune conditions – and is a particularly relevant area of research in understanding the long-term complications of Lyme disease.
Membrane fluidity
The basic unit of all living organisms is the cell, which is surrounded by a cell membrane. This membrane regulates what enters and leaves the cell, enabling the uptake of nutrients, the release of waste products, the secretion of hormones, and communication between cells. The cell membrane consists mainly of a double layer of phospholipids, in which the molecules contain both water-soluble (hydrophilic) and water-repellent (hydrophobic) parts. The fluidity of the membrane, i.e. the mobility of the molecules, is essential for life.
Below a certain temperature, the membrane can become quasi-crystalline, significantly reducing its mobility. At this point, the membrane becomes leaky, loses its functions, and the spatial structure of the proteins it contains changes. This conformational change can be perceived as a “foreign” structure by the immune system, triggering autoimmune reactions.
The role of essential fatty acids
Membrane fluidity is primarily ensured by essential fatty acids, which are bent-chain, polyunsaturated fatty acids. Their deficiency increases the risk of quasi-crystallisation. The body tries to compensate for this by increasing cholesterol levels, as cholesterol enhances membrane fluidity. However, if the deficiency of essential fatty acids is severe, this adaptive mechanism is exhausted and membrane stability is compromised.
A new theory of autoimmunity
During foetal development, the immune system recognises “self” and “non-self” structures based on cell membranes that are still sufficiently fluid. Later, if the fatty acid composition of the cell membrane changes, proteins can take on new conformations that the immune system recognises as foreign. This can lead, for example, to type 1 diabetes (if it attacks the cells of the islets of Langerhans) or rheumatism (if it attacks the joint cells).
The relationship between cholesterol levels and disease
Elevated serum cholesterol does not cause disease on its own, but may be the body’s response to a lack of essential fatty acids. In Western societies, average serum cholesterol levels are constantly rising. This deficiency indicates a risk of quasi-crystallisation of cell membranes and increases the risk of diseases such as atherosclerosis, heart attack or autoimmune diseases.
Infections and membrane fluidity
Some pathogens, such as Borrelia bacteria (the causative agent of Lyme disease), are able to break down the essential fatty acids of the host cell, thereby reducing membrane fluidity. At the same time, the pathogen removes cholesterol from the host cell, thereby stabilising its own membrane. This dual effect is beneficial to the pathogen, as it weakens the immune response and causes the cell to leak, providing nourishment for the bacteria. This process often leads to an autoimmune reaction.
According to the authors’ hypothesis, the increase in cholesterol levels is therefore a natural defence mechanism by which the body attempts to maintain membrane fluidity in the event of an essential fatty acid deficiency.
Summary:
Several mechanisms may therefore be involved in the development of autoimmune diseases.
Molecular mimicry is an immunological phenomenon in which certain proteins of pathogens are structurally similar to the host’s own proteins. This similarity can trigger an erroneous immune response, which can lead to an attack on the body’s own tissues, thus playing a central role in the development of autoimmune diseases such as type 1 diabetes or the autoimmune complications of Lyme disease.
The article examines the development of autoimmune diseases from a new perspective and argues that their main cause is a lack of essential fatty acids and the resulting quasi-crystallisation of membranes. The body tries to compensate for this by increasing cholesterol levels, but this is only a temporary solution. The solution may lie in proper nutrition, antioxidant intake and reducing oxidative stress.
Sources:
https://www.scirp.org/journal/paperinformation?paperid=43791
https://www.pnas.org/doi/10.1073/pnas.1633447100
https://pubmed.ncbi.nlm.nih.gov/22583438/
(C) Lyme Borreliosis Foundation
