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Mentions: The phenomenon of effectors functioning in parallel is common in EPEC . Interestingly, the TTSS mutants (escV) and ΔnleBE were only partially deficient in blocking the TNFα-induced migration of NF-κB to the nucleus, suggesting that an additional TTSS-independent mechanism might function in parallel to NleBE to inhibit translocation of NF-κB to the nucleus (Fig. 7). This activity might be related to damping of the signal due to continuous exposure to PAMPs like flagellin or LPS. Interestingly, the TTSS escV mutant was completely deficient in inhibition of IL8 expression, while the nleBE mutant was only partially deficient in this function. We therefore predict that EPEC encode additional putative effector(s) that function in parallel to NleBE by blocking IL-8 expression (Fig. 7).
The Type III Secretion Effector NleE Inhibits NF-κB Activation
Bottom Line: Importantly, we show that NleE inhibits NF-kappaB activation by preventing activation of IKKbeta and consequently the degradation of the NF-kappaB inhibitor, IkappaB.This NleE activity is enhanced by, but is not dependent on, a second injected effector, NleB.In conclusion, this study describes two effectors, NleB and NleE, with no similarity to other known proteins, used by pathogens to manipulate NF-kappaB signaling pathways.
Affiliation: Department of Microbiology and Molecular Genetics, IMRIC, Faculty of Medicine, The Hebrew University, Jerusalem, Israel.
Abstract: The complex host-pathogen interplay involves the recognition of the pathogen by the host's innate immune system and countermeasures taken by the pathogen. Detection of invading bacteria by the host leads to rapid activation of the transcription factor NF-kappaB, followed by inflammation and eradication of the intruders. In response, some pathogens, including enteropathogenic Escherichia coli (EPEC), acquired means of blocking NF-kappaB activation. We show that inhibition of NF-kappaB activation by EPEC involves the injection of NleE into the host cell. Importantly, we show that NleE inhibits NF-kappaB activation by preventing activation of IKKbeta and consequently the degradation of the NF-kappaB inhibitor, IkappaB. This NleE activity is enhanced by, but is not dependent on, a second injected effector, NleB. In conclusion, this study describes two effectors, NleB and NleE, with no similarity to other known proteins, used by pathogens to manipulate NF-kappaB signaling pathways.
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