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Published on: October 23, 2013
Plasmid-Encoded Pgp5 Is a Significant Contributor to Chlamydia muridarum Induction of Hydrosalpinx
Yumeng Huang1, Qi Zhang2, Zhangsheng Yang3
1Department of Microbiology & Immunology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas, 78229, United States of America; Department of Dermatology, 2nd Xiangya Hospital, Xiangya School of Medicine, Central South University of China, Changsha, Hunan 410013, P. R. China.
Abstract:
We have previously shown that the plasmid-encoded Pgp3 is a major virulence factor for C. muridarum induction of hydrosalpinx. We now report that Pgp5 also plays a significant role in the development of hydrosalpinx following C. muridarum induction. Pgp5 deficiency was introduced via either in-frame deletion (CM-Δpgp5) or premature stop codon installation (CM-pgp5S). Mice infected with either CM-Δpgp5 or CM-pgp5S developed hydrosalpinges at significantly reduced levels with an incidence rate of <40% and a mean severity score of 2 or less. In contrast, 80% or more mice developed hydrosalpinx with a severity score of >3 when mice were infected with Pgp5-sufficient C. muridarum (plasmid-competent wild type or plasmid-free C. muridarum transformed with a full plasmid or depleted of pgp7 gene). The attenuated pathogenicity of the Pgp5-deficient C. muridarum correlated with a significantly reduced level of ascending infection in the oviduct tissue despite the similar overall shedding courses between mice infected with Pgp5-deficient versus sufficient C. muridarum. Furthermore, in the oviducts of mice infected with Pgp5-deficient C. muridarum, significantly lower levels of inflammatory cell infiltration and cytokine production were detected. Thus, Pgp5 is a significant plasmid-encoded virulence factor for C. muridarum pathogenicity in the upper genital tract.
Insights
Chlamydia muridarum Pgp5 protein is a significant virulence factor. Pgp5 deficiency in C. muridarum reduces hydrosalpinx development and upper genital tract infection severity in mice.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Plasmid-encoded Pgp3 is a known virulence factor for Chlamydia muridarum-induced hydrosalpinx.
- The role of other plasmid-encoded proteins in C. muridarum pathogenesis remains to be fully elucidated.
Purpose of the Study:
- To investigate the role of the plasmid-encoded Pgp5 protein in the development of hydrosalpinx following Chlamydia muridarum infection.
- To determine the impact of Pgp5 deficiency on ascending infection, inflammation, and cytokine production in the mouse oviduct.
Main Methods:
- Generation of Pgp5-deficient Chlamydia muridarum strains (CM-Δpgp5 and CM-pgp5S).
- Infection of mice with Pgp5-deficient or Pgp5-sufficient C. muridarum strains.
- Assessment of hydrosalpinx incidence and severity, ascending infection levels, inflammatory cell infiltration, and cytokine production.
Main Results:
- Mice infected with Pgp5-deficient C. muridarum showed significantly reduced hydrosalpinx incidence (<40%) and severity (score ≤2).
- In contrast, Pgp5-sufficient C. muridarum infection led to hydrosalpinx in ≥80% of mice with severity scores >3.
- Pgp5 deficiency correlated with reduced ascending infection, lower inflammatory cell infiltration, and decreased cytokine production in oviduct tissue.
Conclusions:
- Pgp5 is a significant plasmid-encoded virulence factor contributing to Chlamydia muridarum pathogenicity.
- Pgp5 plays a crucial role in the development of hydrosalpinx and ascending infection in the upper genital tract.
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