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Updated: Jun 8, 2026
Experimental Infection with Listeria monocytogenes as a Model for Studying Host Interferon-γ Responses
Published on: November 16, 2016
Transcriptome analysis indicates an enhanced activation of adaptive and innate immunity by chlamydia-infected murine
Katalin Burian1, Valeria Endresz, Judit Deak
1Department of Medical Microbiology and Immunobiology, University of Szeged, Szeged, Hungary.
Background:
Interferon γ (IFN‐γ) is the major cytokine involved in the elimination of Chlamydia infection. Despite its importance, the combined effect of Chlamydia infection and IFN‐γ on the gene expression of murine epithelial cells has only partially been described.
Methods:
The DNA chip method was used to evaluate the impact of IFN‐γ and both the human strain Chlamydia trachomatis L2 infection and the murine strain Chlamydia muridarum infection on the transcriptome of murine epithelial cells.
Results:
The gene expression analysis revealed that IFN‐γ had an enhancing effect on both the up‐regulation and down‐regulation of the epithelial gene expression. The influenced gene functional classes included cytokine and chemokine expression, antigen presentation, apoptosis, and genes involved in basic metabolic processes such as fatty acid oxidation. We also detected the up‐regulation of various genes that could be directly antichlamydial, such as members of the p47 GTPase family, inducible nitric oxide synthase, and monokine induced by IFN‐γ (MIG). As a functional validation of DNA chip data, we measured the antichlamydial effect of MIG on the extracellular form of Chlamydia.
Conclusions:
Our results show that IFN‐γ is a key cytokine that primes epithelial cells to activate adaptive and innate immunity and to express antichlamydial effector genes both intracellularly and extracellularly.
