Affiliation:
1. Institute of Bacterial Infections and Zoonoses
2. Institute of Molecular Pathogenesis, Friedrich-Loeffler-Institut (Federal Research Institute for Animal Health), Jena, Germany
3. Hans Knoell Institute for Natural Products Research, Jena, Germany
Abstract
ABSTRACT
The obligatory intracellular bacterium
Chlamydophila psittaci
is the causative agent of psittacosis in birds and humans. The capability of this zoonotic pathogen to develop a persistent phase is likely to play a role in chronicity of infections, as well as in failure of antibiotic therapy and immunoprophylaxis. To elucidate three different in vitro models for transition of
C. psittaci
to persistence (iron depletion, penicillin G treatment, and gamma interferon [IFN-γ] exposure), a set of 27 genes was examined by mRNA expression analysis using quantitative real-time PCR. While the phenotypical characteristics were the same as in other chlamydiae, i.e., aberrant morphology of reticulate bodies, loss of cultivability, and rescue of infectivity upon removal of inducers, the transcriptional response of
C. psittaci
to persistence-inducing factors included several new and distinctive features. Consistent downregulation of membrane proteins, chlamydial sigma factors, cell division protein, and reticulate body-elementary body differentiation proteins from 24 h postinfection onward proved to be a general feature of
C. psittaci
persistence. However, other genes displayed considerable variations in response patterns from one model to another, which suggests that there is no persistence model per se. In contrast to results for
Chlamydia trachomatis
, late shutdown of essential genes in
C. psittaci
was more comprehensive with IFN-γ-induced persistence, which is probably due to the absence of a functional tryptophan synthesis operon.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
91 articles.
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