Auto Immunity: Campylobacter and the Guillain Barré Syndrome
October 31, 2005 at 2:44 am #2307InuyashaParticipant
Ok please help edit this paper. I need to know what i have to change and better.
Tianyang Guo October 28, 2005
Biology of Infectious Diseases
Auto Immunity: Campylobacter and the Guillain Barré Syndrome
Campylobacter are gram-negative rods that are small, curved, and mobile. They have widths that range from 0.2-0.9 mm, and lengths that range from 0.5-5.0 mm. Exhibiting dart-like motion, Campylobacter are either monotrichous or amphitrichous (having either one flagellum or two flagella). A strong correlation is present between Campylobacter and the development of Guillain Barré Syndrome (GBS). GBS is a polyneuropathy that causes prompt progressive inflammation of the nerves. The syndrome results in a loss of sensation and muscle weakness. It does this by creating the destruction or loss of the myelin sheath of the nerves. Without the myelin sheath, the nerve fibers have no electrical insulator. GBS is also characterized by lymphocytic infiltration (the permeation of the lymph). Similar to other auto-immune disease caused by infections (such as rheumatic fever which is triggered by group A streptococci), the Guillain Barré Syndrome is an autoimmune diseases that has a increased onset when following the infection of Campylobacter.
Using Campylobacter jejuni (C. jejuin) as an example, Campylobacter infections induce antibodies to form. These antibodies cross react and respond to several peripheral nerve antigens. The antibodies attach to the peripheral nerve antigens and result in nerve destruction. Recent studies have confirmed that patients who have GBS often develop antibodies for certain strains of Campylobacter which cross react with gangliosides of the peripheral nerves. Gangliosides are membrane-anchored glycosphingolipids that have a hydrophilic extracellular oligosaccharide. Lipopolysaccharide, a compound or complex of lipid and carbohydrate, formed by certain strains of Campylobacter are structurally similar to the gangliosides found in peripheral nerves. The Campylobacter O:19 serotype, a subdivision of a species that is distinguishable from other strains on the basis of antigenicity, has an identical tetrasaccharide with the GM1 ganglioside found on the peripheral nerves. Campylobacter also has an identical pentasaccharide to the GD1a ganglioside which is also formed on the peripheral nerves. Serotypes O:23 and O:36 from Campylobacter furthermore share a branched tetrasaccharide with the GM2 ganglioside. Infection by Campylobacter correlates with the specificity of cross reactive auto-antibodies. Due to the similarity between the serotypes of Campylobacter and the gangliosides of the peripheral nerves, antibodies produce attach to both. These antibodies then signal the destruction of what they attached too, whether Campylobacter or peripheral nerves.
GBS following infection by Campylobacter is associated with severe clinical course, prominent motor symptoms, and the presence of antibodies to the GM1 ganglioside. Carbohydrate mimicry between the bacterial lipooligosaccharide and human GM1 ganglioside is very important in determining the pathogenesis of Guillain–Barré Syndrome. The anti-GM1 IgG found in patients who had Guillain Barré Syndrome blocked muscle action potentials and resulted in weakened muscle movement. Carbohydrate mimicry is therefore an important cause of auto-immunity. Because Campylobacter has carbohydrates that resemble the gangliosides found on nerves the body actually attacks the nerve system. The body’s immunity can not clearly distinguish between the pathogen and its own nerves. Therefore it attacks its own nerves.
GBS affects the peripheral nerves, the nerve roots, and the cranial nerves. The affects are caused by myelin damage. Nerve tissue can be found infiltrated with certain types of white blood cells. Autoimmune diseases are triggered by acute infections. GBS and rheumatic fever are common examples of autoimmune diseases that are triggered by acute infections from defined microorganisms. Rheumatic fever is triggered by group A streptococci. It affects multiple organs, in particular the heart, joints, kidney, and CNS. GBS is an inflammatory disease of the peripheral nervous system that is triggered by either Campylobacter, Epstein-Barr virus, cytomegalovirus, or Mycoplasma pneumoniae. Campylobacter however is the principal infectious agent that is linked with the development of GBS. In GBS, the involvement of Campylobacter has been documented not only serologically, but also by complete isolation of the bacterium from GBS patients. In a well-controlled study which compared the frequency of positive cultures from patients to that of household controls, Campylobacter was found in 26% of GBS patients and 2% of the controls.
To prove that molecular mimicry results in autoimmune diseases two conditions must be satisfied: (i) pathogen has to be present in a large number of cases; (ii) a detectable immune response due to the pathogen must be present. These conditions have been proved for GBS subsequent to Campylobacter infection. There is proof that Campylobacter uses mimicry and cause GBS. Several Campylobacter strains have been isolated from GBS patients. Mimicry induces the production of pathogenic auto-antibodies and the development of GBS. Molecular mimicry is the mechanism in which an infectious agent triggers an immune response against the body’s own antigens.
Campylobacter induces auto-immunity which causes GBS. By having serotypes that resembled the gangliosides of the peripheral nerves and by using molecular (carbohydrate) mimicry, the human body is provoked into producing antibodies against its own nerves. These antibodies likely signal the destruction of the myelin of these nerves.
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October 31, 2005 at 6:42 am #31866iri_blackParticipant
Very interesting! I like pathology 🙂
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