OspA L03 Group2: Difference between revisions

The Borrelia bacteria has proteins on its surface that are different in immunogenic expression (Wagner, 2012). One of these outer surface proteins, OspA, is a [http://en.wikipedia.org/wiki/Lipoprotein lipoprotein] that was found to inhibit bacterial transmission <ref name=Ding >PMID: 11183781</ref>. OspA, known as a potent stimulator of [http://en.wikipedia.org/wiki/Neutrophils nuetrophils], was able to kill the pathogen and attract [http://en.wikipedia.org/wiki/Leukocytes leukocytes]. The interaction of OspA on the antigen and the antibodies was a cascade [http://en.wikipedia.org/wiki/Complement_system complement system]. Once the complement found OspA on borrelia, it induced an innate response of [http://en.wikipedia.org/wiki/Phagocytosis phagocytosis] allowing the release of [http://en.wikipedia.org/wiki/Proinflammatory_cytokines proinflamatory cytokines] in a host <ref name=Ruprecht >PMID: 18097481</ref> and avoid contracting Lyme disease as it affects the heart, joints, and [http://en.wikipedia.org/wiki/Central_nervous_system central nervous sytem] <ref name=Ruprecht >PMID: 18097481</ref>.

Once entered the host through the skin or blood stream, Borrelia burgdorferi downregulated and suppressed OspA to minimize all of the host’s [http://en.wikipedia.org/wiki/Immunogenic 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 [http://en.wikipedia.org/wiki/Apoptosis apoptosis] on the bacteria through the activation of [http://en.wikipedia.org/wiki/B-cells B-cells] <ref name=Ruprecht >PMID: 18097481</ref>.