Alison J Eastman1, Ingrid L Bergin2, Daniel Chai3, Christine M Bassis4, William LeBar5, George O Oluoch3, Emma R Liechty2, Atunga Nyachieo3, Vincent B Young4, David M Aronoff6, Dorothy L Patton7, Jason D Bell1. 1. Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor. 2. Unit for Laboratory Animal Medicine, University of Michigan, Ann Arbor. 3. Institute of Primate Research, National Museum of Kenya, Karen. 4. Division of Infectious Diseases, Department of Internal Medicine, University of Michigan, Ann Arbor. 5. Department of Pathology, University of Michigan, Ann Arbor. 6. Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee. 7. Department of Obstetrics and Gynecology, University of Washington, Seattle.
Abstract
Background: Understanding the relationship between the levonorgestrel (LNG)-releasing intrauterine system (IUS) and sexually transmitted infections (STIs) is increasingly important as use of the LNG-IUS grows to include women at higher risk for STIs. This study assessed the impact of the LNG-IUS on development of Chlamydia trachomatis pelvic inflammatory disease, using a baboon model. Methods: Baboons with and those without the LNG-IUS were cervically inoculated with C. trachomatis and monitored daily, and cervical and fallopian tube swab specimens were collected weekly for C. trachomatis quantitation by nucleic acid amplification testing and culture. Vaginal swab specimens were collected for cytokine analysis, and serum samples were obtained for detection of C. trachomatis antibodies. Results: The LNG-IUS resulted in an increased C. trachomatis burden in the cervix, with the bacterial burden in the LNG-IUS group diverging from that in the non-LNG-IUS group by 6 weeks after infection. One of 7 baboons in the non-LNG-IUS group and 2 of 6 in the LNG-IUS group developed pelvic inflammatory disease, while 3 animals in each group met criteria suggestive of pelvic inflammatory disease. LNG-IUS increased baseline interleukin 8 levels but failed to further upregulate interleukin 8 during infection. In LNG-IUS recipients, early perturbations in the interleukin 1β axis corresponded to decreased C. trachomatis clearance and increased T-helper type 2 immune responses. Conclusion: LNG-IUS use results in delayed clearance of C. trachomatis and might alter the reproductive tract immune environment.
Background: Understanding the relationship between the levonorgestrel (LNG)-releasing intrauterine system (IUS) and sexually transmitted infections (STIs) is increasingly important as use of the LNG-IUS grows to include women at higher risk for STIs. This study assessed the impact of the LNG-IUS on development of Chlamydia trachomatis pelvic inflammatory disease, using a baboon model. Methods:Baboons with and those without the LNG-IUS were cervically inoculated with C. trachomatis and monitored daily, and cervical and fallopian tube swab specimens were collected weekly for C. trachomatis quantitation by nucleic acid amplification testing and culture. Vaginal swab specimens were collected for cytokine analysis, and serum samples were obtained for detection of C. trachomatis antibodies. Results: The LNG-IUS resulted in an increased C. trachomatis burden in the cervix, with the bacterial burden in the LNG-IUS group diverging from that in the non-LNG-IUS group by 6 weeks after infection. One of 7 baboons in the non-LNG-IUS group and 2 of 6 in the LNG-IUS group developed pelvic inflammatory disease, while 3 animals in each group met criteria suggestive of pelvic inflammatory disease. LNG-IUS increased baseline interleukin 8 levels but failed to further upregulate interleukin 8 during infection. In LNG-IUS recipients, early perturbations in the interleukin 1β axis corresponded to decreased C. trachomatis clearance and increased T-helper type 2 immune responses. Conclusion: LNG-IUS use results in delayed clearance of C. trachomatis and might alter the reproductive tract immune environment.
Authors: Jason D Bell; Ingrid L Bergin; Lisa H Harris; Daniel Chai; Isaac Mullei; Jason Mwenda; Vanessa K Dalton; Anjel Vahratian; William Lebar; Melissa K Zochowski; Nicholas Kiulia; David M Aronoff; Dorothy L Patton Journal: J Infect Dis Date: 2011-09-15 Impact factor: 5.226
Authors: S A Hashway; I L Bergin; C M Bassis; M Uchihashi; K C Schmidt; V B Young; D M Aronoff; D L Patton; J D Bell Journal: J Med Primatol Date: 2013-11-23 Impact factor: 0.667
Authors: S Menon; S H Stansfield; M Walsh; E Hope; L Isaia; A A Righarts; T Niupulusu; S V A Temese; L Iosefa-Siitia; L Auvaa; S A Tapelu; M F Motu; T Suaalii-Sauni; P Timms; P C Hill; W M Huston Journal: BMC Infect Dis Date: 2016-04-21 Impact factor: 3.090
Authors: Jordan K Kyongo; Vicky Jespers; Odin Goovaerts; Johan Michiels; Joris Menten; Raina N Fichorova; Tania Crucitti; Guido Vanham; Kevin K Ariën Journal: PLoS One Date: 2012-08-31 Impact factor: 3.240
Authors: Gregory Spear; Kristina Rothaeulser; Linda Fritts; Patrick M Gillevet; Christopher J Miller Journal: PLoS One Date: 2012-12-28 Impact factor: 3.240