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Analysis of Inflammasome Gene Regulation Following Chlamydia pneumoniae Infection of THP1 Monocytes: Implications for Alzheimer’s Disease
Research Day
  • Jonathan M. Anzman, Philadelphia College of Osteopathic Medicine
  • Christine J. Hammond, Philadelphia College of Osteopathic Medicine
  • Brian J. Balin, Philadelphia College of Osteopathic Medicine
Location
Philadelphia Campus
Start Date
2-5-2012 2:00 PM
End Date
2-5-2012 4:00 PM
Description
Background: Neuroinflammation has been found to be characteristic of neurological diseases, including Alzheimer’s disease. Research focusing on the cause of Alzheimer’s disease has produced evidence that chronic infection(s) may be at the root of the problem. Our lab has shown that the bacterium Chlamydia pneumoniae can infect many different types of cells in the brain and manipulate them so as to survive intracellularly for long periods of time. Furthermore, Chlamydia pneumoniae is known to illicit a prominent pro-inflammatory response during infection. In recent years the pathways associated with the release of pro-inflammatory cytokines, such as IL-6 and IL-1β, have been uncovered. The innate immune system initially responds to disruptive agents by releasing pro-inflammatory cytokines and initiating the inflammatory process. The purpose of this process is to control the disturbance and prevent any further damage to the body. When an infection is unable to be quickly controlled, the inflammatory process can have deleterious effects. At the heart of these pathways are inflammasomes, which initiate cytokine release when foreign substances are detected, leading to inflammation.
Citation Information
Jonathan M. Anzman, Christine J. Hammond and Brian J. Balin. "Analysis of Inflammasome Gene Regulation Following Chlamydia pneumoniae Infection of THP1 Monocytes: Implications for Alzheimer’s Disease" (2012)
Available at: http://works.bepress.com/christine_hammond/9/