OspA L03 Group2: Difference between revisions

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Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

Chris DiFiore, Yimei Miao, Kareema Roushdy, Michal Harel

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+=='''About OspA'''==
-Specifically, outer surface protein A, or OspA is found to inhibit bacterial transmission <ref name=Ding >PMID: 11183781</ref>. Outer surface protein A, or OspA was found to initiate an immune response that contributed towards the development of Lyme disease vaccinations. It prevented the transmission of [http://en.wikipedia.org/wiki/Borrelia_burgdorferi Borrelia_burgdorferi], the causative bacterial agent of Lyme disease after the attachment of an infected tick <ref name=Ding >PMID: 11183781</ref>.
+Borrelia bacteria differntially immunogenic express outer surface proteins (Wagner, 2012). One outersurface protein, OspA is a lipoprotein that was found to inhibit bacterial transmission <ref name=Ding >PMID: 11183781</ref>. The interaction of OspA on the antigen and the antibodies was a cascade complement system. Once the complement found OspA on borrelia, it induced an innate response of [http://en.wikipedia.org/wiki/Phagocytosis phagocytosis]. Not only did OspA allowed opsonization, but also attracted [http://en.wikipedia.org/wiki/White_blood_cell leukocytes] (<ref name=Ding >PMID: 11183781</ref>.
-=='''About OspA'''==
+ In order for Lyme Disease to start and progress in the human or animal body, the initial levels of OspA is underregulated, inactivated, hidden, or OspA negative <ref name=Ding >PMID: 11183781</ref>. The bacteria underregulates OspA for the reason that it does not want to trigger any innate immune response from the host <ref name=Ding >PMID: 11183781</ref>.
-OspA is a lipoprotein found on the outer surface of the bacteria that is found to inhibit bacterial transmission <ref name=Ding >PMID: 11183781</ref>.  In order for Lyme Disease to start and progress in the human or animal body, the initial levels of OspA is underregulated, inactivated, hidden, or OspA negative <ref name=Ding >PMID: 11183781</ref>. The bacteria underregulates OspA for the reason that it does not want to trigger any innate immune response from the host <ref name=Ding >PMID: 11183781</ref>.
-The whole system of OspA on the antigen interacting with the antibodies was a cascade complement system. Once the complement found OspA on borrelia, it induced an innate response of [http://en.wikipedia.org/wiki/Phagocytosis phagocytosis]. Not only did OspA allowed opsonization, but also attracted [http://en.wikipedia.org/wiki/White_blood_cell leukocytes] (<ref name=Ding >PMID: 11183781</ref>.
+==== Pathology of OspA ====
+Once entered the host through the skin or blood stream, Borrelia burgdorferi downregulated and suppressed OspA to minimize all of the host’s immunogenic characteristics <ref name=Ruprecht >PMID: 18097481</ref>, while expression of OspC was active. Usually, the initial stages of Lyme disease diagnosed individuals with peaked elevations of OspC up until 7-11 weeks, then later declined (Wagner, 2012). When OspA on the spirochete migrated to an inflammatory environment, it induced apoptosis on the bacteria through the activation of B-cells <ref name=Ruprecht >PMID: 18097481</ref>. OspA known as a potent stimulator of neutrophils was able to kill the pathogen and attract leukocytes allowing the release of proinflammatory cytokines in a host <ref name=Ruprecht >PMID: 18097481</ref> and avoid contracting Lyme disease as it affects the heart, joints, and central nervous system <ref name=Ruprecht >PMID: 18097481</ref>.
-==== Pathology of OspA ====
-Once entered the host through the skin or blood stream, Borrelia burgdorferi downregulated and suppressed OspA to minimize all of the host’s immunogenic characteristics <ref name=Ruprecht >PMID: 18097481</ref>. When OspA on the spirochete migrated to an inflammatory environment, it induced apoptosis on the bacteria through the activation of B-cells <ref name=Ruprecht >PMID: 18097481</ref>. Only OspA positive in borrelia bacteria were unable to establish an infection compared to OspA negative bacteria successfully hosted in studies of mice <ref name=Ruprecht >PMID: 18097481</ref>. OspA known as a potent stimulator of neutrophils was able to kill the pathogen and attract leukocytes allowing the release of proinflammatory cytokines in a host <ref name=Ruprecht >PMID: 18097481</ref> and avoid contracting Lyme disease as it affects the heart, joints, and central nervous system <ref name=Ruprecht >PMID: 18097481</ref>.
 The reactive LA-2 antibody was found to serve as an important [http://en.wikipedia.org/wiki/Epitope epitope] of Osp-A binding <ref name=Ding >PMID: 11183781</ref> towards developing vaccinations. The free state of the 3D model exposed the C-terminal where there were 49 residues from the “three loops” involved that significantly affected by LA-2 binding, through findings from nuclear magnetic resonance, or [http://en.wikipedia.org/wiki/Nuclear_magnetic_resonance  NMR] and [http://en.wikipedia.org/wiki/Protein_crystallization crystallization] <ref name=Ding >PMID: 11183781</ref>.