NS 3310 1st Edition Lecture 11Outline of Past LectureI. TCA CycleII. Oxidative PhosphorylationIII. Glucose MetabolismOutline of Current LectureI. Theories of IBD PathogenesisII. IBD in Boxer DogsCurrent LectureI. Theories of IBD Pathogenesis- Possible causes:-Luminal microbes- specific pathogen, dysbiosis-Mucosal barrier- altered mucus layer, permeability changes, cellular starvation, and impaired epithelial repair-Host genetic defects- impaired bacterial sensing, defective bacterial killing, defunct cell signaling, reduced autophagy, mucosal barrier defects-Defective immunoregulation- abnormal Ag processing, loss of tolerance, defective apoptosis, aggressive T cell responses- Host-microbe interactions have shaped the genetic architecture of IBDThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.II. IBD in Boxer Dogs- 9/30 boxer dogs affected- Bacteria visualized in ulcerated mucosa and clinical responses of 6/9 dogs - No infection agent consistently identified- Bacteria in ulcerated mucosa considered secondary invaders- Categorized as idiopathic immune mediated- After 40 years of excessive immunosuppression, successful management of histiocytic ulcerative colitis with enroflaxacin in two Boxer dogs- Granulomatous Colitis of boxer dogs associated with increased intramucosal bacteria- When these dogs treated with antibiotics, the condition goes away- There are common genes associated with this disease- French bulldogs also have this disease; they have a genetic linkage with boxers - GCB pathogenesis in bulldogs ultimately caused by opportunistic E.coli, defective bacterial killing and inflammatory trigger- Floral shifts are a consequence of intestinal inflammation- Genetic defects associated with IBD impact the threshold and magnitude of floral
View Full Document