User:Marvin O'Neal/OspA: Difference between revisions
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Lyme disease is a debilitating condition that begins with a characteristic bullseye rash known as an [http://en.wikipedia.org/wiki/Erythema_chronicum_migrans erythema migrans (EM)] as well as the development of lesions on other parts of the body, not just at the site of the tick's attachment to its host. Secondary stage symptoms include affecting the heart, joints, and both the central and peripheral nervous systems. <i>Borrelia</i> | Lyme disease is a debilitating condition that begins with a characteristic bullseye rash known as an [http://en.wikipedia.org/wiki/Erythema_chronicum_migrans erythema migrans (EM)] as well as the development of lesions on other parts of the body, not just at the site of the tick's attachment to its host. Secondary stage symptoms include affecting the heart, joints, and both the central and peripheral nervous systems. OspA is used in adhering to the tick's gut by binding with the tick receptor for OspA (TROSPA), a receptor necessary for the colonization of <i>Borrelia</i> inside the tick. High levels of both OspA and TROSPA are found prior to feeding, but are downregulated once the feeding process begins in order to initiate transmission into the host.<ref name="pal">PMID: 15537536</ref> | ||
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While feeding, OspA is downregulated in order to evade an immune response from the incoming host blood into the gut, releasing the <i>Borrelia</i> from the gut wall and migrating into the tick's salivary glands, thereby allowing it to enter the host through the bite. This is evidenced by the fact that patients with Lyme disease have been found to not possess OspA antibodies in the early stages of the disease.<ref name="connolly">PMID: 15864264</ref><ref name="rupprecht">PMID: 18097481</ref> OspA is the protein most related to acute Lyme neuroborreliosis (LNB), the neurological manifestations of Lyme disease. | |||
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Once inside the host, the <i>Borrelia</i> has a great number of mechanisms available to actively suppress the host's immune system response and neutralize its effector mechanisms, such as the expression of another outer surface protein, OspC, which prevents susceptibility to the host's [http://en.wikipedia.org/wiki/Innate_immune_system innate immunity] and [http://en.wikipedia.org/wiki/Complement_system complement systems]. Additionally, <i>Borrelia</i> is capable of suppressing many of its surface proteins to reduce its detectability, but can also utilize protective means by temporarily expressing them when needed.</p> | Once inside the host, the <i>Borrelia</i> has a great number of mechanisms available to actively suppress the host's immune system response and neutralize its effector mechanisms, such as the expression of another outer surface protein, OspC, which prevents susceptibility to the host's [http://en.wikipedia.org/wiki/Innate_immune_system innate immunity] and [http://en.wikipedia.org/wiki/Complement_system complement systems]. Additionally, <i>Borrelia</i> is capable of suppressing many of its surface proteins to reduce its detectability, but can also utilize protective means by temporarily expressing them when needed.</p> | ||
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<h2>OspA | <h2>OspA's Role in Lyme Disease</h2> | ||
<h3>Acute Lyme Neuroborreliosis (LNB)</h3> | |||
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Acute Lyme Neuroborreliosis (LNB) is part of the second stage of Lyme disease in which the spirochete invades the peripheral and central nervous systems (CNS). Symptoms of LNB include: Bannwarth’s | Acute Lyme Neuroborreliosis (LNB) is part of the second stage of Lyme disease in which the spirochete invades the peripheral and central nervous systems (CNS). Symptoms of LNB include: meningoradiculitis with inflammation of the nerve roots and [http://en.wikipedia.org/wiki/Radicular_pain radiculitis] (Bannwarth’s syndrome), lymphocytic meningitis, and cranial and [http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001619/ peripheral neuritis]. In Europe, the strain predominantly found in the CSF of patients with Bannwarth's syndrome is <i>B. garinii</i>. However, in the United States, Bannwarth's syndrome is rare and the most common manifestations of Lyme neuroborreliosis is [http://en.wikipedia.org/wiki/Meningitis meningitis], caused by <i>B. burgdorferi</i>. The presence of OspA in the cerebrospinal fluid (CSF) is responsible for this complex inflammatory response in the brain that leads to the neuroborreliosis.<ref name="rupprecht">PMID: 18097481</ref> | ||
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<h3>Role in Inflammation</h3> | |||
[[Image:G2L03-OspA-mechanism.jpg|thumb|300px|Mechanism of the host inflammatory response to OspA]] | [[Image:G2L03-OspA-mechanism.jpg|thumb|300px|Mechanism of the host inflammatory response to OspA]] | ||
