Journal article
Host nectin-1 is required for efficient Chlamydia trachomatis serovar E development
Frontiers in cellular and infection microbiology, Vol.4, pp.158-158
2014
Handle:
https://hdl.handle.net/2376/101725
PMCID: PMC4222120
PMID: 25414835
Abstract
Interaction of Herpes Simplex Virus (HSV) glycoprotein D (gD) with the host cell surface during Chlamydia trachomatis/HSV co-infection stimulates chlamydiae to become persistent. During viral entry, gD interacts with one of 4 host co-receptors: HVEM (herpes virus entry mediator), nectin-1, nectin-2 and 3-O-sulfated heparan sulfate. HVEM and nectin-1 are high-affinity entry receptors for both HSV-1 and HSV-2. Nectin-2 mediates HSV-2 entry but is inactive for HSV-1, while 3-O-sulfated heparan sulfate facilitates HSV-1, but not HSV-2, entry. Western blot and RT-PCR analyses demonstrate that HeLa and HEC-1B cells express nectin-1 and nectin-2, but not HVEM. Because both HSV-1 and HSV-2 trigger persistence, these data suggest that nectin-1 is the most likely co-receptor involved. Co-infections with nectin-1 specific HSV-1 mutants stimulate chlamydial persistence, as evidenced by aberrant body (AB) formation and decreased production of elementary bodies (EBs). These data indicate that nectin-1 is involved in viral-induced chlamydial persistence. However, inhibition of signal transduction molecules associated with HSV attachment and entry does not rescue EB production during C. trachomatis/HSV-2 co-infection. HSV attachment also does not activate Cdc42 in HeLa cells, as would be expected with viral stimulated activation of nectin-1 signaling. Additionally, immunofluorescence assays confirm that HSV infection decreases nectin-1 expression. Together, these observations suggest that gD binding-induced loss of nectin-1 signaling negatively influences chlamydial growth. Chlamydial infection studies in nectin-1 knockdown (NKD) HeLa cell lines support this hypothesis. In NKD cells, chlamydial inclusions are smaller in size, contain ABs, and produce significantly fewer infectious EBs compared to C. trachomatis infection in control HeLa cells. Overall, the current study indicates that the actions of host molecule, nectin-1, are required for successful C. trachomatis development.
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Details
- Title
- Host nectin-1 is required for efficient Chlamydia trachomatis serovar E development
- Creators
- Jennifer V Hall - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University Johnson City, TN, USA ; Center for Inflammation, Infectious Disease and Immunity, Quillen College of Medicine, East Tennessee State University Johnson City, TN, USAJingru Sun - College of Medical Sciences, Washington State University Spokane, WA, USAJessica Slade - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University Johnson City, TN, USA ; Center for Inflammation, Infectious Disease and Immunity, Quillen College of Medicine, East Tennessee State University Johnson City, TN, USAJennifer Kintner - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University Johnson City, TN, USAMarissa Bambino - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University Johnson City, TN, USAJudy Whittimore - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University Johnson City, TN, USARobert V Schoborg - Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University Johnson City, TN, USA ; Center for Inflammation, Infectious Disease and Immunity, Quillen College of Medicine, East Tennessee State University Johnson City, TN, USA
- Publication Details
- Frontiers in cellular and infection microbiology, Vol.4, pp.158-158
- Academic Unit
- Biomedical Sciences, Department of
- Publisher
- Switzerland
- Grant note
- R01 AI095637 / NIAID NIH HHS R01 AI095637-01 / NIAID NIH HHS
- Identifiers
- 99900546557201842
- Language
- English
- Resource Type
- Journal article