Did you see some one before who can fly without wings or move without legs? You will answer : definitely no, but I know someone, or better yet some living thing, who can do just both and it is called Borrelia burgdorferi; let’s share its story. It is a loosely coiled bacterium belonging to a class called spirochetes (moving bacteria).

Borrelia burgdorferi

Borrelia burgdorferi is motile through the undulation of its axial filaments. It is transmitted to humans by the bite of infected ticks (Ixodes scapularis and Ixodes pacificus) and cause a serious progressive disease called lyme disease.

The story of lyme disease began in 1975 when a mother, with her children in lyme city in the United States, was admitted to a hospital with signs of rheumatoid arthritis. It was a mysterious case until the discovery of Borrelia burgdorferi and that is how the disease got its name, when it was discovered in 1982. Symptoms and signs of lyme disease can be categorized into three phases:

Phase (1): An early localized skin rash, characterized by inflamed red edges with a clear white center at the site of insect bite, appears and is called “erythema migrans“.

Erythema migrans

Phase (2): The rash resolves as the bacteria begin to move into the blood stream towards their target organs like large joints, heart, and nervous system.

Phase (3): Inflammation of heart muscle leads to abnormal rhythm, meningitis, confusion and finally arthritis.

Treatment in the early phase is an easy mission by amoxicillin or doxycycline, orally for few weeks. However, the recommended regimen in late stages include parenteral ceftriaxone, analgesics to control the severe pain, and anti-inflammatory drugs, usually required for months .

Images credits:
Borrelia burgdorferi: http://www.wadsworth.org/databank/hirez/hechemy2.gif
Erythema migrans: http://phil.cdc.gov/PHIL_Images/9875/9875_lores.jpg

Not too long ago, I read about a research done at the Kennedy Institute of Rheumatology Division, which has identified a new ligand for Toll-like receptor 4. This receptor was previously known for activating the immune system through the detection of threats as lipopolysaccharide or gram-negative bacteria. The new ligand, Tenascin-C, is an extracellular glycoprotein, whose elevated expression in cases of inflammation provoked scientists to study its role in the process.

The study noted that its presence was critical to maintain the ongoing inflammation seen in cases of rheumatoid arthritis. In reference to this study, the author stated “We have uncovered one way that the immune system may be triggered to attack the joints in patients with rheumatoid arthritis. We hope our new findings can be used to develop new therapies that interfere with tenascin-C activation of the immune system and that these will reduce the painful inflammation that is a hallmark of this condition”

I was able to contact Dr Kim Midwood and obtained this brief interview:

The researchers have found two proteins “IL-15 and PDGF” which are needed to cause activation & proliferation of T-cells. IL-15 causes activation, while PDGF stimulates their growth.

Another signaling protein called “NFκB” controlled by the two proteins which prevent the death of cancer cells whatever they are over expressed.All those proteins may become targets for drugs; when they blocked NFκB with drugs in cells from leukemia patients, an increase in mortality of abnormal T-cells has been observed.

So, the key is to find out what stimulates T-cells to survive & proliferate.

Source: Science Daily.

Image credits:  Immune response.