Abstract
suppressed nuclear translocation of NFκB compared to non-invasive E. coli strains and LPS at 30 min post infection. However, unlike non-invasive E. coli strains, 13I and LF82 infection resulted in chronic activation of NF κB. Summary: CD-associated AIEC strains replicate within macrophages by initially suppressing NFκB activation. However, bacterial replication within macrophages induces chronic activation of NF κB, which correlates with increased TNF-α secretion from infected macrophages. Conclusion:Modulation of intracellular signaling pathways by invading CD-associated E. coli strains could contribute to an initial survival advantage and eventual chronic inflammation, as seen in CD.
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