Literature DB >> 12142274

The chlamydial inclusion: escape from the endocytic pathway.

Kenneth A Fields1, Ted Hackstadt.   

Abstract

Chlamydiae, bacterial obligate intracellular pathogens, are the etiologic agents of several human diseases. A large part of the chlamydial intracellular survival strategy involves the formation of a unique organelle called the inclusion that provides a protected site within which they replicate. The chlamydial inclusion is effectively isolated from endocytic pathways but is fusogenic with a subset of exocytic vesicles that deliver sphingomyelin from the Golgi apparatus to the plasma membrane. A combination of host and parasite functions contribute to the biogenesis of this compartment. Establishment of the mature inclusion is accompanied by the insertion of multiple chlamydial proteins, suggesting that chlamydiae actively modify the inclusion to define its interactions with the eukaryotic host cell. Despite being sequestered within a membrane-bound vacuole, chlamydiae clearly communicate with and manipulate the host cell from within this privileged intracellular niche.

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Year:  2002        PMID: 12142274     DOI: 10.1146/annurev.cellbio.18.012502.105845

Source DB:  PubMed          Journal:  Annu Rev Cell Dev Biol        ISSN: 1081-0706            Impact factor:   13.827


  94 in total

1.  Tarp and Arp: How Chlamydia induces its own entry.

Authors:  Joanne Engel
Journal:  Proc Natl Acad Sci U S A       Date:  2004-06-29       Impact factor: 11.205

2.  Native properdin binds to Chlamydia pneumoniae and promotes complement activation.

Authors:  Claudio Cortes; V P Ferreira; Michael K Pangburn
Journal:  Infect Immun       Date:  2010-12-06       Impact factor: 3.441

3.  SNARE motif: a common motif used by pathogens to manipulate membrane fusion.

Authors:  Jordan Wesolowski; Fabienne Paumet
Journal:  Virulence       Date:  2010 Jul-Aug       Impact factor: 5.882

4.  Analysis of putative Chlamydia trachomatis chaperones Scc2 and Scc3 and their use in the identification of type III secretion substrates.

Authors:  Kenneth A Fields; Elizabeth R Fischer; David J Mead; Ted Hackstadt
Journal:  J Bacteriol       Date:  2005-09       Impact factor: 3.490

Review 5.  Role of sphingolipids in microbial pathogenesis.

Authors:  Lena J Heung; Chiara Luberto; Maurizio Del Poeta
Journal:  Infect Immun       Date:  2006-01       Impact factor: 3.441

6.  Inhibition of chlamydiae by primary alcohols correlates with the strain-specific complement of plasticity zone phospholipase D genes.

Authors:  David E Nelson; Deborah D Crane; Lacey D Taylor; David W Dorward; Morgan M Goheen; Harlan D Caldwell
Journal:  Infect Immun       Date:  2006-01       Impact factor: 3.441

7.  Treatment of Chlamydia trachomatis with a small molecule inhibitor of the Yersinia type III secretion system disrupts progression of the chlamydial developmental cycle.

Authors:  K Wolf; H J Betts; B Chellas-Géry; S Hower; C N Linton; K A Fields
Journal:  Mol Microbiol       Date:  2006-09       Impact factor: 3.501

8.  Absence of Specific Chlamydia trachomatis Inclusion Membrane Proteins Triggers Premature Inclusion Membrane Lysis and Host Cell Death.

Authors:  Mary M Weber; Jennifer L Lam; Cheryl A Dooley; Nicholas F Noriea; Bryan T Hansen; Forrest H Hoyt; Aaron B Carmody; Gail L Sturdevant; Ted Hackstadt
Journal:  Cell Rep       Date:  2017-05-16       Impact factor: 9.423

9.  Chlamydia pneumoniae replicates in Kupffer cells in mouse model of liver infection.

Authors:  Antonella Marangoni; Manuela Donati; Francesca Cavrini; Rita Aldini; Silvia Accardo; Vittorio Sambri; Marco Montagnani; Roberto Cevenini
Journal:  World J Gastroenterol       Date:  2006-10-28       Impact factor: 5.742

10.  Generation of genetic diversity in microsporidia via sexual reproduction and horizontal gene transfer.

Authors:  Soo Chan Lee; Louis M Weiss; Joseph Heitman
Journal:  Commun Integr Biol       Date:  2009-09
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