Differential transcriptional responses between the interferon-gamma-induction and iron-limitation models of persistence for Chlamydia pneumoniae
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Peter Timms1, David Good, Charles Wan
1School of Life Sciences, Queensland University of Technology, Institute of Health and Biomedical Innovation, Brisbane, Australia. p.timms@qut.edu.au
Background And Purpose:
Chlamydia spp. are important pathogens of humans and animals that cause a wide range of acute and chronic infections. A persistence model has been developed in which Chlamydia spp. do not complete their developmental cycle, have significantly reduced infectivity for new host cells, and exhibit abnormal inclusion and reticulate body morphology. This study was performed to compare the interferon-gamma (IFN-gamma) induction and iron-limitation models of persistence for Chlamydia spp. to investigate the common and unique transcriptional pathways involved.
Methods:
A quantitative real time-polymerase chain reaction approach was used to compare the IFN-gamma induction and iron-limitation models of Chlamydia pneumoniae persistence at the transcriptional level by analyzing selected genes in each of 5 distinct, functionally relevant subcategories.
Results:
The models showed minimal evidence of a general transcriptional stress response in persistence, with only 1 of the 7 genes analyzed in the IFN-gamma induction model (htrA) and 4 of the genes in the iron-limitation model (htrA, clpB, clpP1, ahpC) showing increased mRNA levels. Both models showed similar responses in relation to the genes associated with lack of reticulate body to elementary body conversion (ctcB, lcrH1, and hctB levels were all unchanged or downregulated). The models also showed similar responses to the key cell wall/envelope genes, ompA, omcB, and crpA, exhibiting lower mRNA levels in both models.
Conclusions:
These data show that several key transcriptional pathways (lack of late developmental cycle completion, key cell wall components) respond similarly between the models. However, other pathways appear to differ depending on the persistence-inducing mechanism. This result suggests that Chlamydia spp. have evolved more than 1 mechanism to respond to different persistence-inducing conditions, but ultimately the pathways probably converge through a common persistence regulon.
Insights
Chlamydia persistence involves shared transcriptional pathways for developmental cycle completion and cell wall maintenance, despite differing responses to interferon-gamma or iron limitation. This suggests multiple Chlamydia spp. survival strategies converging on a common regulon.
Area of Science:
- Microbiology
- Molecular Biology
- Pathogen Research
Background:
- Chlamydia spp. are significant human and animal pathogens causing diverse infections.
- A Chlamydia persistence model involves incomplete developmental cycles, reduced infectivity, and altered morphology.
- Interferon-gamma (IFN-gamma) induction and iron limitation are known triggers for Chlamydia persistence.
Purpose of the Study:
- To compare transcriptional pathways involved in IFN-gamma induction and iron-limitation models of Chlamydia persistence.
- To identify common and unique gene expression patterns under different persistence-inducing conditions.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) was employed.
- Transcriptional levels of selected genes were analyzed in both IFN-gamma and iron-limitation persistence models.
- Genes were categorized into 5 functionally relevant subcategories.
Main Results:
- Minimal general transcriptional stress response observed; only specific genes (htrA, clpB, clpP1, ahpC) showed increased mRNA in persistence models.
- Both models exhibited similar downregulation or unchanged levels of genes related to reticulate body to elementary body conversion (ctcB, lcrH1, hctB).
- Key cell wall/envelope genes (ompA, omcB, crpA) showed reduced mRNA levels in both persistence models.
Conclusions:
- Shared transcriptional responses in Chlamydia persistence involve developmental cycle completion and cell wall component regulation.
- Distinct pathways are modulated depending on the specific persistence-inducing mechanism (IFN-gamma vs. iron limitation).
- Chlamydia spp. likely utilize multiple adaptive strategies that converge on a common persistence regulatory network.
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