What is the mechanism by which Campylobacter jejuni leads to Guillain-Barre syndrome?

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Campylobacter jejuni is known to be associated with Guillain-Barre syndrome (GBS) primarily through its role in inducing an autoimmune response. After infection with Campylobacter jejuni, the body mounts an immune response against the bacterial antigens. Some of these antigens are structurally similar to components found in human peripheral nerves, a phenomenon known as molecular mimicry. When the immune system targets these bacterial components, it can inadvertently attack the nervous system, leading to demyelination and neurological symptoms characteristic of Guillain-Barre syndrome.

This autoimmune process typically occurs after gastrointestinal illness caused by the bacteria, highlighting the connection between the infection and the subsequent development of GBS. Understanding this mechanism underscores the importance of recognizing and treating Campylobacter infections promptly to potentially mitigate the risk of autoimmune complications such as GBS.

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