Lipid acquisition by intracellular Chlamydiae
Summary Chlamydia species are obligate intracellular pathogens that are important causes of human genital tract, ocular and respiratory infections. The bacteria replicate within a specialized membrane‐bound compartment termed the inclusion and require host‐derived lipids for intracellular growth and...
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| Published in | Cellular microbiology Vol. 14; no. 7; pp. 1010 - 1018 |
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| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Publishing Ltd
01.07.2012
Hindawi Limited |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Summary
Chlamydia species are obligate intracellular pathogens that are important causes of human genital tract, ocular and respiratory infections. The bacteria replicate within a specialized membrane‐bound compartment termed the inclusion and require host‐derived lipids for intracellular growth and development. Emerging evidence indicates that Chlamydia has evolved clever strategies to fulfil its lipid needs by interacting with multiple host cell compartments and redirecting trafficking pathways to its intracellular niche. In this review, we highlight recent findings that have significantly expanded our understanding of how Chlamydia exploit lipid trafficking pathways to ensure the survival of this important human pathogen. |
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| AbstractList | Chlamydia
species are obligate intracellular pathogens that are important causes of human genital tract, ocular, and respiratory infections. The bacteria replicate within a specialized membrane-bound compartment termed the inclusion and require host-derived lipids for intracellular growth and development. Emerging evidence indicates that
Chlamydia
has evolved clever strategies to fulfill its lipid needs by interacting with multiple host cell compartments and redirecting trafficking pathways to its intracellular niche. In this review, we highlight recent findings that have significantly expanded our understanding of how
Chlamydia
exploit lipid trafficking pathways to ensure the survival of this important human pathogen. Chlamydia species are obligate intracellular pathogens that are important causes of human genital tract, ocular and respiratory infections. The bacteria replicate within a specialized membrane-bound compartment termed the inclusion and require host-derived lipids for intracellular growth and development. Emerging evidence indicates that Chlamydia has evolved clever strategies to fulfil its lipid needs by interacting with multiple host cell compartments and redirecting trafficking pathways to its intracellular niche. In this review, we highlight recent findings that have significantly expanded our understanding of how Chlamydia exploit lipid trafficking pathways to ensure the survival of this important human pathogen. Summary Chlamydia species are obligate intracellular pathogens that are important causes of human genital tract, ocular and respiratory infections. The bacteria replicate within a specialized membrane-bound compartment termed the inclusion and require host-derived lipids for intracellular growth and development. Emerging evidence indicates that Chlamydia has evolved clever strategies to fulfil its lipid needs by interacting with multiple host cell compartments and redirecting trafficking pathways to its intracellular niche. In this review, we highlight recent findings that have significantly expanded our understanding of how Chlamydia exploit lipid trafficking pathways to ensure the survival of this important human pathogen. [PUBLICATION ABSTRACT] Summary Chlamydia species are obligate intracellular pathogens that are important causes of human genital tract, ocular and respiratory infections. The bacteria replicate within a specialized membrane‐bound compartment termed the inclusion and require host‐derived lipids for intracellular growth and development. Emerging evidence indicates that Chlamydia has evolved clever strategies to fulfil its lipid needs by interacting with multiple host cell compartments and redirecting trafficking pathways to its intracellular niche. In this review, we highlight recent findings that have significantly expanded our understanding of how Chlamydia exploit lipid trafficking pathways to ensure the survival of this important human pathogen. |
| Author | Engel, Joanne N. Elwell, Cherilyn A. |
| AuthorAffiliation | 3 Department of Microbial Pathogenesis and Host Defense Program 2 Department of Microbiology and Immunology 1 Department of Medicine |
| AuthorAffiliation_xml | – name: 1 Department of Medicine – name: 2 Department of Microbiology and Immunology – name: 3 Department of Microbial Pathogenesis and Host Defense Program |
| Author_xml | – sequence: 1 givenname: Cherilyn A. surname: Elwell fullname: Elwell, Cherilyn A. – sequence: 2 givenname: Joanne N. surname: Engel fullname: Engel, Joanne N. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22452394$$D View this record in MEDLINE/PubMed |
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| Snippet | Summary
Chlamydia species are obligate intracellular pathogens that are important causes of human genital tract, ocular and respiratory infections. The... Chlamydia species are obligate intracellular pathogens that are important causes of human genital tract, ocular and respiratory infections. The bacteria... Summary Chlamydia species are obligate intracellular pathogens that are important causes of human genital tract, ocular and respiratory infections. The... Chlamydia species are obligate intracellular pathogens that are important causes of human genital tract, ocular, and respiratory infections. The bacteria... |
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| SubjectTerms | Chlamydia Chlamydia - growth & development Chlamydia - metabolism Genital tract Humans Inclusion Bodies - microbiology Infection Lipid Metabolism Lipids Pathogens |
| Title | Lipid acquisition by intracellular Chlamydiae |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1462-5822.2012.01794.x https://www.ncbi.nlm.nih.gov/pubmed/22452394 https://www.proquest.com/docview/1020478510 https://search.proquest.com/docview/1020828914 https://search.proquest.com/docview/1024659540 https://pubmed.ncbi.nlm.nih.gov/PMC3376245 |
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