Plasmid-Encoded Pgp5 Is a Significant Contributor to Chlamydia muridarum Induction of Hydrosalpinx.
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.
Department 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.
Yumeng
Y
Huang
Department 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 Obstetrics and Gynecology, 3rd Xiangya Hospital, Xiangya School of Medicine, Central South University of China, Changsha, Hunan 410013, P. R. China.
Qi
Q
Zhang
Department of Microbiology & Immunology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas, 78229, United States of America.
Zhangsheng
Z
Yang
Department of Microbiology & Immunology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas, 78229, United States of America.
Turner
T
Conrad
Department 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 Dermatovenereology, Tianjin Medical University General Hospital, 154 Anshan Rd., Tianjin 300052, P. R. China.
Yuanjun
Y
Liu
Department of Microbiology & Immunology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas, 78229, United States of America.
Guangming
G
Zhong
D000818:Animals; D002690:Chlamydia Infections / Q000382:microbiology*; D023502:Chlamydia muridarum / Q000235:genetics / Q000472:pathogenicity*; D005187:Fallopian Tubes / Q000382:microbiology*; D005260:Female; D006023:Glycoproteins / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D010957:Plasmids / Q000235:genetics; D037521:Virulence Factors / Q000235:genetics / Q000378:metabolism*
D006023:Glycoproteins; D037521:Virulence Factors