دورية أكاديمية

Type three secretion system-mediated escape of Burkholderia pseudomallei into the host cytosol is critical for the activation of NFkappaB.

التفاصيل البيبلوغرافية
العنوان: Type three secretion system-mediated escape of Burkholderia pseudomallei into the host cytosol is critical for the activation of NFkappaB.
المؤلفون: Boon Eng Teh, French, Christopher Todd, Yahua Chen, Gek Joo Chen, Isabelle, Ting-Hsiang Wu, Sagullo, Enrico, Pei-Yu Chiou, Teitell, Michael A., Miller, Jeff F., Yunn-Hwen Gan
المصدر: BMC Microbiology; 2014, Vol. 14 Issue 1, p1-27, 27p
مصطلحات موضوعية: BURKHOLDERIA pseudomallei, CYTOSOL, SECRETION, GRAM-negative bacteria, MELIOIDOSIS
مصطلحات جغرافية: SOUTHEAST Asia, NORTHERN Australia
مستخلص: Background Burkholderia pseudomallei is the causative agent of melioidosis, a potentially fatal disease endemic in Southeast Asia and Northern Australia. This Gram-negative pathogen possesses numerous virulence factors including three “injection type” type three secretion systems (T3SSs). B. pseudomallei has been shown to activate NFκB in HEK293T cells in a Toll-like receptor and MyD88 independent manner that requires T3SS gene cluster 3 (T3SS3 or T3SSBsa). However, the mechanism of how T3SS3 contributes to NFκB activation is unknown. Results Known T3SS3 effectors are not responsible for NFκB activation. Furthermore, T3SS3-null mutants are able to activate NFκB almost to the same extent as wildtype bacteria at late time points of infection, corresponding to delayed escape into the cytosol. NFκB activation also occurs when bacteria are delivered directly into the cytosol by photothermal nanoblade injection. Conclusions T3SS3 does not directly activate NFκB but facilitates bacterial escape into the cytosol where the host is able to sense the presence of the pathogen through cytosolic sensors leading to NFκB activation. [ABSTRACT FROM AUTHOR]
Copyright of BMC Microbiology is the property of BioMed Central and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
قاعدة البيانات: Complementary Index
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Academic Journal
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Array ( [Name] => Abstract [Label] => Abstract [Group] => Ab [Data] => Background Burkholderia pseudomallei is the causative agent of melioidosis, a potentially fatal disease endemic in Southeast Asia and Northern Australia. This Gram-negative pathogen possesses numerous virulence factors including three “injection type” type three secretion systems (T3SSs). B. pseudomallei has been shown to activate NFκB in HEK293T cells in a Toll-like receptor and MyD88 independent manner that requires T3SS gene cluster 3 (T3SS3 or T3SSBsa). However, the mechanism of how T3SS3 contributes to NFκB activation is unknown. Results Known T3SS3 effectors are not responsible for NFκB activation. Furthermore, T3SS3-null mutants are able to activate NFκB almost to the same extent as wildtype bacteria at late time points of infection, corresponding to delayed escape into the cytosol. NFκB activation also occurs when bacteria are delivered directly into the cytosol by photothermal nanoblade injection. Conclusions T3SS3 does not directly activate NFκB but facilitates bacterial escape into the cytosol where the host is able to sense the presence of the pathogen through cytosolic sensors leading to NFκB activation. [ABSTRACT FROM AUTHOR] )
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