Increased S-Nitrosylation and Proteasomal Degradation of Caspase-3 during Infection Contribute to the Persistence of AIEC
- Thread starter kiny
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kiny
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I think this part is interesting. Their ability to quickly replicate isn't just the issue, it's their ability to stay alive within immune cells by avoiding apoptosis, coupled with genetic autophagy defects in specific crohn's disease ATG genes like NOD2, ATG16L1, IRGM...etc. Their ability to stay alive for extremely long periods would make crohn's disease a chronic disease.
"Therefore the possible presence of a sub-population of persistent cells within the AIEC population cannot be over looked. Persister cells, an increasingly resistant sub-population of bacteria that develop during infection, have been described for other pathogens especially those that form biofilms [62]. For AIEC persister cells may play a crucial role in maintaining a percentage of the macrophage and DC population infected and in a heightened inflammatory state. These AIEC upon their release from infected cells could act as a seeding mechanism for further infection, contributing to the persistent nature of infection as is seen in CD. In this regard rapid intracellular replication as previously reported may not be as important as the ability to persist within immune cells"
I think it's interesting that many people on the forum say that cipro worked for a while and then stopped working. Cipro is pretty good at killing E coli, it's also macrophage penetrating, but no matter what common antibiotic you use, you would run into resistance after a while.
"Therefore the possible presence of a sub-population of persistent cells within the AIEC population cannot be over looked. Persister cells, an increasingly resistant sub-population of bacteria that develop during infection, have been described for other pathogens especially those that form biofilms [62]. For AIEC persister cells may play a crucial role in maintaining a percentage of the macrophage and DC population infected and in a heightened inflammatory state. These AIEC upon their release from infected cells could act as a seeding mechanism for further infection, contributing to the persistent nature of infection as is seen in CD. In this regard rapid intracellular replication as previously reported may not be as important as the ability to persist within immune cells"
I think it's interesting that many people on the forum say that cipro worked for a while and then stopped working. Cipro is pretty good at killing E coli, it's also macrophage penetrating, but no matter what common antibiotic you use, you would run into resistance after a while.
