User:Marvin O'Neal/OspA: Difference between revisions

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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.   
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>






<h2>OspA's Role in Lyme Disease</h2>
<h2>OspA's Role in Invasion</h2>
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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.
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<h3>Acute Lyme Neuroborreliosis (LNB)</h3>
<h3>Acute Lyme Neuroborreliosis (LNB)</h3>
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<h3>Evasion and the Extracellular Matrix</h3>
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The <i>Borrelia</i> are able to hide in the [http://en.wikipedia.org/wiki/Extracellular_matrix extracellular matrix], allowing it to survive by avoiding [http://en.wikipedia.org/wiki/Leukocytes leukocytes] circulating in the bloodstream. OspA can rapidly bind to plasminogen, which becomes [http://en.wikipedia.org/wiki/Plasmin plasmin] once activated, and degrades the extracellular matrix. By binding to plasminogen, <i>Borrelia</i> could be utilizing its function to invade the extracellular matrix. However, due to the fact that OspA is downregulated during biting, and stays unexpressed, there might be another potential mechanism instead. Additionally, <i>Borrelia</i> induces the local upregulation of matrix metalloproteinase-9, causing the digestion of the surrounding extracellular matrix. <i>Borrelia</i> can also bind to several proteins in the extracellular matrix, such as [http://en.wikipedia.org/wiki/Fibronectin fibronectin], [http://en.wikipedia.org/wiki/Integrins integrins] or [http://en.wikipedia.org/wiki/Decorin decorin], which can aid in the spread and survival of the spirochetes in these tissues.
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<h3>Role in Inflammation</h3>
<h3>Role in Inflammation</h3>