当前位置： SCI文献检索 > Cell Host & Microbe期刊下所有文献 > Impaired stimulation of p38α-MAPK/Vps41-HOPS by LPS from pathogenic Coxiella burnetii prevents trafficking to microbicidal phagolysosomes.

Impaired stimulation of p38α-MAPK/Vps41-HOPS by LPS from pathogenic Coxiella burnetii prevents trafficking to microbicidal phagolysosomes.

Abstract：

:Variations in lipopolysaccharide (LPS), a bacterial outer membrane component, determine virulence of the obligate intracellular bacterium Coxiella burnetii, but the underlying mechanisms are unknown. We find that while avirulent C. burnetii LPS (avLPS) stimulates host p38α-MAPK signaling required for proper trafficking of bacteria containing compartments to lysosomes for destruction, pathogenic C. burnetii LPS (vLPS) does not. The defect in vLPS and pathogenic C. burnetii targeting to degradative compartments involves an antagonistic engagement of TLR4 by vLPS, lack of p38α-MAPK-driven phosphorylation, and block in recruitment of the homotypic fusion and protein-sorting complex component Vps41 to vLPS-containing vesicles. An upstream activator of p38α-MAPK or phosphomimetic mutant Vps41-S796E expression overrides the inhibition, allowing vLPS and pathogenic C. burnetii targeting to phagolysosomes. Thus, p38α-MAPK and its crosstalk with Vps41 play a central role in trafficking bacteria to phagolysosomes. Pathogenic C. burnetii has evolved LPS variations to evade this host response and thrive intracellularly.

journal_name

Cell Host Microbe

journal_title

Cell host & microbe

authors

Barry AO,Boucherit N,Mottola G,Vadovic P,Trouplin V,Soubeyran P,Capo C,Bonatti S,Nebreda A,Toman R,Lemichez E,Mege JL,Ghigo E

doi

10.1016/j.chom.2012.10.015

subject

Has Abstract

pub_date

2012-12-13 00:00:00

pages

751-63

issue

6

eissn

1931-3128

issn

1934-6069

pii

S1931-3128(12)00364-2

journal_volume

12

pub_type

杂志文章

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