scholarly journals Modulation of cytokines and transcription factors (T-Bet and GATA3) in CD4 enriched cervical cells of Chlamydia trachomatis infected fertile and infertile women upon stimulation with chlamydial inclusion membrane proteins B and C

2009 ◽  
Vol 7 (1) ◽  
pp. 84 ◽  
Author(s):  
Rishein Gupta ◽  
Harsh Vardhan ◽  
Pragya Srivastava ◽  
Sudha Salhan ◽  
Aruna Mittal
Cell Reports ◽  
2017 ◽  
Vol 19 (7) ◽  
pp. 1406-1417 ◽  
Author(s):  
Mary M. Weber ◽  
Jennifer L. Lam ◽  
Cheryl A. Dooley ◽  
Nicholas F. Noriea ◽  
Bryan T. Hansen ◽  
...  

2008 ◽  
Vol 76 (6) ◽  
pp. 2746-2757 ◽  
Author(s):  
Zhongyu Li ◽  
Chaoqun Chen ◽  
Ding Chen ◽  
Yimou Wu ◽  
Youmin Zhong ◽  
...  

ABSTRACT Although the Chlamydia trachomatis genome is predicted to encode 50 inclusion membrane proteins, only 18 have been experimentally localized in the inclusion membrane of C. trachomatis-infected cells. Using fusion proteins and anti-fusion protein antibodies, we have systematically evaluated all 50 putative inclusion membrane proteins for their localization in the infected cells, distribution patterns, and effects on subsequent chlamydial infection when expressed ectopically, as well as their immunogenicity during chlamydial infection in humans. Twenty-two of the 50 proteins were localized in the inclusion membrane, and 7 were detected inside the inclusions, while the location of the remaining 21 was not defined. Four (CT225, CT228, CT358, and CT440) of the 22 inclusion membrane-localized proteins were visualized in the inclusion membrane of Chlamydia-infected cells for the first time in the current study. The seven intra-inclusion-localized proteins were confirmed to be chlamydial organism proteins in a Western blot assay. Further characterization of the 50 proteins revealed that neither colocalization with host cell endoplasmic reticulum nor inhibition of subsequent chlamydial infection by ectopically expressed proteins correlated with the inclusion membrane localization. Interestingly, antibodies from women with C. trachomatis urogenital infection preferentially recognized proteins localized in the inclusion membrane, and the immunodominant regions were further mapped to the region predicted to be on the cytoplasmic side of the inclusion membrane. These observations suggest that most of the inclusion membrane-localized proteins are both expressed and immunogenic during C. trachomatis infection in humans and that the cytoplasmic exposure may enhance the immunogenicity.


1999 ◽  
Vol 33 (4) ◽  
pp. 753-765 ◽  
Author(s):  
Marci A. Scidmore-Carlson ◽  
Edward I. Shaw ◽  
Cheryl A. Dooley ◽  
Elizabeth R. Fischer ◽  
Ted Hackstadt

2019 ◽  
Vol 25 (S2) ◽  
pp. 1166-1167
Author(s):  
Benjamin Crews ◽  
Elizabeth R. Fischer ◽  
Forrest Hoyt ◽  
Bryan T. Hansen ◽  
Ted Hackstadt

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Erika I. Lutter ◽  
Craig Martens ◽  
Ted Hackstadt

Chlamydiaspp. are obligate intracellular pathogens that replicate within a vacuole termed the inclusion. Chlamydiae extensively modify the inclusion membrane via the insertion of chlamydial inclusion membrane proteins (Incs) which decorate the cytosolic face of the inclusion. We have assessed the overall relatedness and phylogeny of Incs in order to identify potential evolutionary trends. Despite a high degree of conservation among Incs withinC. trachomatisserovars, phylogenetic analysis showed that some Incs cluster according to clinical groupings suggesting that certain Incs may contribute to tissue tropism. Bioinformatic predictions identified Incs in five chlamydial species: 55 inC. trachomatis, 68 inC. felis, 92 inC. pneumoniae, 79 inC. caviae, and 54 inC. muridarum. Inc homologues were compared between chlamydial species and 23 core Incs were identified as shared among all species. Genomic expansion of Incs was identified inC. pneumoniae, C. caviae, andC. felisbut notC. trachomatisorC. muridarum.


2015 ◽  
Vol 83 (12) ◽  
pp. 4710-4718 ◽  
Author(s):  
Mary M. Weber ◽  
Laura D. Bauler ◽  
Jennifer Lam ◽  
Ted Hackstadt

Chlamydia trachomatisis an obligate intracellular pathogen that replicates in a membrane-bound vacuole termed the inclusion. Early in the infection cycle, the pathogen extensively modifies the inclusion membrane through incorporation of numerous type III secreted effector proteins, called inclusion membrane proteins (Incs). These proteins are characterized by a bilobed hydrophobic domain of 40 amino acids. The presence of this domain has been used to predict up to 59 putative Incs forC. trachomatis; however, localization to the inclusion membrane with specific antibodies has been demonstrated for only about half of them. Here, we employed recently developed genetic tools to verify the localization of predicted Incs that had not been previously localized to the inclusion membrane. Expression of epitope-tagged putative Incs identified 10 that were previously unverified as inclusion membrane localized and thus authentic Incs. One novel Inc and 3 previously described Incs were localized to inclusion membrane microdomains, as evidenced by colocalization with phosphorylated Src (p-Src). Several predicted Incs did not localize to the inclusion membrane but instead remained associated with the bacteria. UsingYersiniaas a surrogate host, we demonstrated that many of these are not secreted via type III secretion, further suggesting they may not be true Incs. Collectively, our results highlight the utility of genetic tools for demonstrating secretion from chlamydia. Further mechanistic studies aimed at elucidating effector function will advance our understanding of how the pathogen maintains its unique intracellular niche and mediates interactions with the host.


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