Murine Vaginal Co-infection with Penicillinase-Producing Neisseria gonorrhoeae Fails to Alleviate Amoxicillin-Induced Chlamydial Persistence
D. Onorini, C. A. Leonard, T. Pesch, B. Prähauser, R. V. Schoborg, N. Borel
Abstract
Chlamydia trachomatis (CT) and Neisseria gonorrhoeae (NG) cause most bacterial sexually transmitted infections (STIs) worldwide. CT/NG co-infection is more common than expected due to chance, suggesting CT/NG interaction. However, CT/NG co-infection remains largely unstudied. Obligate intracellular CT has a characteristic biphasic developmental cycle consisting of two bacterial forms, infectious elementary bodies (EBs) and non-infectious, replicating reticulate bodies (RBs), which reside within host-derived, membrane-bound intracellular inclusions. Diverse stressors cause divergence from the normal chlamydial developmental cycle to an aberrant state called chlamydial persistence. Persistence can be induced by host-specific factors such as intracellular nutrient deprivation or cytokine exposure, and exogenous factors such as beta-lactam exposure, which disrupts RB to EB conversion. Persistent chlamydiae are atypical in appearance and, as such, are called aberrant bodies (ABs), but remain viable. The primary hallmark of persistence is reversibility of this temporary non-infectious state; upon removal of the stressor, persistent chlamydiae re-enter normal development, and production of infectious EBs resumes. The beta-lactam amoxicillin (AMX) has been shown to induce chlamydial persistence in a murine vaginal infection model, using the mouse pathogen C. muridarum (CM) to model human CT infection. This remains, to date, the sole experimentally tractable in vivo model of chlamydial persistence. Recently, we found that penicillinase-producing NG (PPNG) can alleviate AMX-induced CT and CM persistence in vitro. We hypothesized that PPNG vaginal co-infection would also alleviate AMX-induced CM persistence in mice. To evaluate this hypothesis, we modified the CM/AMX persistence mouse model, incorporating CM/PPNG co-infection. Contradicting our hypothesis, and recent in vitro findings, PPNG vaginal co-infection failed to alleviate AMX-induced CM persistence.
02 /Specification & Classification
Click any tag to browse matching papers- Organism
- Assay
- Research Focus
- Approach
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- The vaginal microbiota shape local and systemic inflammation during Chlamydia trachomatis infection in non-human primate.
Cindy Adapen, Louis Réot, … Elisabeth Menu·bioRxiv·Feb 20, 2025
- Inhibition of tRNA Synthetases Induces Persistence in Chlamydia
N. D. Hatch, S. P. Ouellette·bioRxiv·Sep 5, 2019
- Murine modeling of menstruation identifies immune correlates of protection during Chlamydia muridarum challenge.
Laurel A. Lawrence, M Elliott Williams, … Alison Swaims-Kohlmeier·PLoS PathogensPeer-reviewed·Jun 6, 2025
- Assaying Chlamydia pneumoniae persistence in monocyte-derived macrophages identifies schisandrin lignans as phenotypic switchers
E. Taavitsainen, M. Kortesoja, L. Hanski·bioRxiv·Jul 19, 2019
- IFNγ and antibody synergize to enhance protective immunity against Chlamydia dissemination and female reproductive tract reinfections
J. I. Gann, P. A. Malaviarachchi, … L.-X. Li·bioRxiv·Aug 4, 2022
- Assessment of Antimicrobial Therapy in Eradicating Chlamydia muridarum in Research Mice: Immune Status and its Impact on Outcomes
Michael B Palillo, Sebastian E. Carrasco, … Rodolfo J Ricart Arbona·Journal of the American Association for Laboratory Animal SciencePeer-reviewed·Oct 22, 2024