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Transcriptional profiling of Rickettsia prowazekii coding and non-coding transcripts during in vitro host-pathogen
Casey L C Schroeder1, Hema P Narra1, Abha Sahni1
1Department of Pathology, University of Texas Medical Branch, 301 University Boulevard Galveston, TX 77555, USA.
Ticks and Tick-Borne Diseases
|July 16, 2017
Summary
This study reveals that Rickettsia prowazekii small RNAs (Rp_sRs) and coding genes show different expression patterns in human versus tick cells. This finding offers new insights into bacterial virulence and transmission dynamics.
Area of Science:
- Microbiology
- Molecular Biology
- Genomics
Background:
- Rickettsia prowazekii causes epidemic typhus and transmits via arthropods.
- Small RNAs (sRNAs) regulate bacterial virulence and adaptation.
- The sRNA expression profile of R. prowazekii in different host cells is largely unknown.
Purpose of the Study:
- To investigate the sRNA expression profile of R. prowazekii during infection of arthropod host cells.
- To compare sRNA and coding gene expression in human and tick host cells.
- To gain insights into rickettsial virulence and transmission.
Main Methods:
- In vitro infection models using human microvascular endothelial cells (HMECs) and Amblyomma americanum (AAE2) cells.
- Strand-specific RNA sequencing for global transcriptome analysis.
- Quantitative RT-PCR for expression profiling of selected sRNAs and genes.
Main Results:
- Identified 67 cis-acting and 26 trans-acting Rp_sRs during AAE2 cell infection.
- Four selected Rp_sRs showed significantly higher expression in tick AAE2 cells compared to HMECs.
- >150 rickettsial genes were differentially expressed between HMECs and AAE2 cells.
- Evidence for host cell-dependent alternative transcription start sites in 18 rickettsial genes.
Conclusions:
- R. prowazekii exhibits distinct sRNA and coding gene expression profiles in human and tick host cells.
- The bacterium utilizes alternative transcription start sites in a host-dependent manner.
- These findings enhance understanding of rickettsial virulence and transmission mechanisms.

