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Transcription of seven genes in a model of interferon‑γ-induced persistent Chlamydia psittaci infection
Zhixi Chen1, Lili Chen1, Chuan Wang1
1Institute of Pathogenic Biology, Medical College, University of South China, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, Hengyang, Hunan 421001, P.R. China.
Abstract:
The obligate intracellular bacterium Chlamydia psittaci is the causative agent of psittacosis in birds and humans. The capability of this zoonotic pathogen to develop a persistent phase may serve a role in the chronicity of infections, in addition to the failure of antibiotic therapy or immunoprophylaxis. In the present study, a C. psittaci strain 6BC persistent infection cell model was induced using interferon (IFN)‑γ, alterations in the infectivity and morphology of the pathogen were analyzed, and the transcript profile of seven selected genes was analyzed. Following treatment with IFN‑γ, the infectivity of C. psittaci 6BC was decreased, the inclusion bodies appeared to be smaller, reticulate bodies were larger and the number of infectious elementary bodies was decreased compared with acute infection. In IFN‑γ‑induced persistently infected cells, the relative mRNA expression levels of the genes CPSIT‑0208, CPSIT‑0310, CPSIT‑0846, CPSIT‑0844 and CPSIT‑0594 were upregulated at 2‑48 h post‑infection (p.i.). The genes CPSIT‑0959 and CPSIT‑0057 were downregulated at 2‑36 h p.i. The results of the present study advanced the understanding of C. psittaci persistent infection and demonstrated a number of previously unknown alterations in chlamydial gene expression, which may provide novel targets to further analyze this particular host‑pathogen interaction.
Insights
Interferon-gamma (IFN-γ) induces a persistent Chlamydia psittaci infection model, altering pathogen morphology and decreasing infectivity. This study reveals key gene expression changes during persistent C. psittaci infections, offering potential therapeutic targets.
Area of Science:
- Microbiology
- Pathogen Biology
- Infectious Diseases
Background:
- Chlamydia psittaci is an obligate intracellular bacterium causing psittacosis in birds and humans.
- Persistent infection by C. psittaci may contribute to chronic illness and treatment failure.
- Understanding persistent C. psittaci infections is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the effects of interferon-gamma (IFN-γ) on C. psittaci 6BC infection.
- To analyze alterations in C. psittaci infectivity, morphology, and gene expression during persistent infection.
- To identify potential novel targets for host-pathogen interaction studies.
Main Methods:
- Induction of a C. psittaci 6BC persistent infection cell model using IFN-γ.
- Analysis of pathogen infectivity and inclusion body morphology.
- Quantitative analysis of mRNA expression for seven selected C. psittaci genes.
Main Results:
- IFN-γ treatment reduced C. psittaci 6BC infectivity and the number of infectious elementary bodies.
- Persistent infection altered chlamydial morphology: smaller inclusion bodies and larger reticulate bodies.
- Upregulation of genes CPSIT‑0208, CPSIT‑0310, CPSIT‑0846, CPSIT‑0844, CPSIT‑0594, and downregulation of CPSIT‑0959, CPSIT‑0057 were observed.
Conclusions:
- IFN-γ effectively induces a persistent C. psittaci infection model with distinct morphological and infectivity changes.
- Significant alterations in chlamydial gene expression occur during persistent infection.
- These identified gene expression changes offer potential targets for future research into C. psittaci host-pathogen interactions.