The Complexities of Lyme Disease (Part 4): Lyme Receptors

This is Part 4 in the series The Complexities of Lyme Disease by Thomas Grier, M.S. Click here to read Part 1. Here to read Part 2. And here to read Part 3.

Lyme Receptors 

It now appears that there are specific receptors in the Lyme spirochete to attach to endothelial
cells, N-Acetyl-glucasomine, B-cells, glial cells, nerves, and neurons.

The way our immune system is supposed to work is that it recognizes foreign invaders as being different from self, and it attacks the infection. Unfortunately, the immune system sometimes attacks our own cells. This is called autoimmune disease. If a foreign invader has a chemical structure similar to our own tissue antigens, our bodies sometimes make antibodies against our own tissues. In people with Lyme disease, scientists have discovered auto-antibodies against our own tissues, including:

• Nerve Cells (Axons)
• Cardiolipin 
• Myelin (also seen in MS)
• Myelin Basic Protein (also seen in MS)
• Neurons (brain cells)

When the immune system finds a foreign invader, it tags that invader in a number of ways. A cell called the macrophage can engulf the bacteria and then communicate to other immune cells the exact description of the bacteria. Another cell might mark the cell with an antibody, which attracts killer T-cells. Some types of T-cells communicate to other cells what to attack and regulates the immune assault. But sometimes, the body can produce a type of antibody that doesn't attack or help. A blocking antibody will attach and coat the intruder, but it won't fix *compliment, and it shields the bacteria from further immune recognition. In Lyme, we have seen quantities of IgG4 blocking antibody such as is seen in some parasitic infections (Tom Schwann RML 92 LDF Conference).

[* Note: Compliment is a term used for a series of 18 + digestive proteins that are only activated by signals from our immune system, such as complement-fixing antibodies that attach to foreign antigens.]

In order for the immune system to make an attacking antibody, the immune system must first find an antigen that it can attack. Unfortunately, as seen by freeze-fracture electron microscope, photographs of the Lyme bacteria show that most of the antigens are on the inside of the inner membrane and not on the outside. This makes the bacteria less visible to the immune system and more difficult to attack.

The most intriguing fact about Borrelia spirochetes is their well-documented ability to change the shape of their surface antigens when they are attacked by the human immune system. When this occurs, it takes several weeks for the immune system to produce new antibodies. During this time, the infection continues to divide and hide. It appears that Borrelia are able to change their surface antigens many times and can do it quickly.

Borrelia burgdorferi (Bb) correlates with the enhancement of Toll-like 

receptor 2 (TLR2) expression by microglia 

American Society for Microbiology

In one study by Dr. Andrew Pachner, M.D., he infected mice with a single strain of Borrelia burgdorferi. After several weeks he was able to isolate two slightly different forms of the bacteria. The bacteria from the bloodstream was attacked and killed by the mouse's immune sera, but the bacteria isolated from the mouse's brain was unaffected by the immune sera. The bacteria isolated from the mouse's brain had a new set of surface antigens.

It appears that contact with the CNS caused the bacteria to change its appearance. Since the brain is isolated from the immune system and is an immune-privileged site, the bacteria became its own separate strain.

This means: Infections of the bloodstream may be different from the infections that are sequestered in the brain. While we continue to have active immunity in the bloodstream, the brain has no immune defenses except for circulating antibodies. So if those circulating antibodies are ineffective to attack the bacteria in the brain, then the brain is left without any defenses, and the infection goes unabated.

Another peculiar observation of this bacteria is seen inside the bacteria. When the genetic control mechanisms of this bacteria are inhibited with antibiotics known as DNA Gyrase Inhibitors (ciprofloxin), the bacteria start to produce bacteriophage.

A phage is a virus that specifically attacks bacteria. In this case, there are two distinct forms. This means the Lyme bacteria at one time was attacked by viruses; it was able to suppress them, but the DNA to make the phage is still incorporated within the DNA of the bacteria. Perhaps activation of this phage could one day be beneficial to treating chronic Lyme patients?

The Complexities of Lyme Disease ( A Microbiology Tutorial) by Thomas Grier, M.S.