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Published on: July 26, 2019
Chlamydia Infection Across Host Species Boundaries Promotes Distinct Sets of Transcribed Anti-Apoptotic Factors
Joshua E Messinger1, Emmalin Nelton1, Colleen Feeney1
1Department of Biology, Ithaca College Ithaca, NY, USA.
Abstract:
Chlamydiae, obligate intracellular bacteria, cause significant human and veterinary associated diseases. Having emerged an estimated 700-million years ago, these bacteria have twice adapted to humans as a host species, causing sexually transmitted infection (C. trachomatis) and respiratory associated disease (C. pneumoniae). The principle mechanism of host cell defense against these intracellular bacteria is the induction of cell death via apoptosis. However, in the "arms race" of co-evolution, Chlamydiae have developed mechanisms to promote cell viability and inhibit cell death. Herein we examine the impact of Chlamydiae infection across multiple host species on transcription of anti-apoptotic genes. We found mostly distinct patterns of gene expression (Mcl1 and cIAPs) elicited by each pathogen-host pair indicating Chlamydiae infection across host species boundaries does not induce a universally shared host response. Understanding species specific host-pathogen interactions is paramount to deciphering how potential pathogens become emerging diseases.
Insights
Chlamydiae bacteria evade host cell death by inhibiting apoptosis. This study reveals distinct gene expression patterns in different host species, showing Chlamydiae infection does not trigger a universal host response.
Area of Science:
- Microbiology
- Immunology
- Evolutionary Biology
Background:
- Chlamydiae are obligate intracellular bacteria causing significant human and veterinary diseases.
- These ancient bacteria have adapted to humans twice, leading to C. trachomatis and C. pneumoniae infections.
- Host cells defend against Chlamydiae by inducing apoptosis, but these bacteria have evolved to inhibit cell death.
Purpose of the Study:
- To investigate the impact of Chlamydiae infection on anti-apoptotic gene transcription across diverse host species.
- To determine if Chlamydiae infection elicits a conserved host response regarding cell viability mechanisms.
Main Methods:
- Analysis of host gene expression patterns, specifically focusing on anti-apoptotic genes like Mcl1 and cIAPs.
- Comparative study across different host-pathogen pairs to identify conserved or distinct transcriptional responses.
Main Results:
- Chlamydiae infection induced largely distinct patterns of anti-apoptotic gene expression (Mcl1 and cIAPs) in different host species.
- No universally shared host transcriptional response was observed across all pathogen-host interactions studied.
Conclusions:
- Chlamydiae employ species-specific strategies to manipulate host cell apoptosis.
- Understanding these unique host-pathogen interactions is crucial for identifying emerging infectious diseases.
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