Taxonomic group: bacteria / Chlamydiae
(Phylum: Chlamydiae)
Associated disease: infection due to Chlamydia trachomatis [ICD11:
XN4Q4 
]
NCBI PubMed ID: 37255490Publication DOI: 10.1128/iai.00096-23Journal NLM ID: 0246127Publisher: American Society for Microbiology
Correspondence: D.D. Rockey <rockeyd
oregonstate.edu>
Institutions: Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, National Institute of Allergy and Infectious Disease, Rocky Mountain Laboratory, Hamilton, Montana, USA, Division of Allergy and Infectious Diseases, Department of Medicine, University of Washington, Seattle, Washington, Department of Medical Microbiology and Infectious Diseases, University of Manitoba Winnipeg, Winnipeg, Manitoba, Canada, Department of Biomedical Sciences, Oregon State University, Corvallis, Oregon, USA
All members of the family Chlamydiaceae have lipopolysaccharides (LPS) that possess a shared carbohydrate trisaccharide antigen, 3-deoxy-d-manno-oct-2-ulosonic acid (Kdo) that is functionally uncharacterized. A single gene, genus-specific epitope (gseA), is responsible for attaching the tri-Kdo to lipid IVA. To investigate the function of Kdo in chlamydial host cell interactions, we made a gseA-null strain (L2ΔgseA) by using TargeTron mutagenesis. Immunofluorescence microscopy and immunoblotting with a Kdo-specific monoclonal antibody demonstrated that L2ΔgseA lacked Kdo. L2ΔgseA reacted by immunoblotting with a monoclonal antibody specific for a conserved LPS glucosamine-PO4 epitope, indicating that core lipid A was retained by the mutant. The mutant strain produced a similar number of inclusions as the parental strain but yielded lower numbers of infectious elementary bodies. Transmission electron microscopy of L2ΔgseA-infected cells showed atypical developmental forms and a reduction in the number of elementary bodies. Immunoblotting of dithiothreitol-treated L2ΔgseA-infected cells lysates revealed a marked reduction in outer membrane OmcB disulfide cross-linking, suggesting that the elementary body outer membrane structure was affected by the lack of Kdo. Notably, lactic acid dehydrogenase release by infected cells demonstrated that L2ΔgseA was significantly more cytotoxic to host cells than the wild type. The cytotoxic phenotype may result from an altered outer membrane biogenesis structure and/or function or, conversely, from a direct pathobiological effect of Kdo on an unknown host cell target. These findings implicate a previously unrecognized role for Kdo in host cell interactions that facilitates postinfection host cell survival.
Lipopolysaccharide, Chlamydia, mutant, TargeTron
Structure type: oligomer
Location inside paper: Fig. 2A
Trivial name: core-lipid A
Compound class: LPS
Contained glycoepitopes: IEDB_130650,IEDB_130657,IEDB_130658,IEDB_130659,IEDB_135394,IEDB_137340,IEDB_141807,IEDB_150760,IEDB_150908,IEDB_151531,IEDB_176772,IEDB_534865
Methods: Western blotting, TEM, genome sequencing, immunofluorescence, LDH assay
NCBI Taxonomy refs (TaxIDs): 813
Show glycosyltransferases
There is only one chemically distinct structure:
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